Research progress of pattern recognition receptors and chronic periodontitis

Pattern recognition receptor(PRR)is a kind of sensor which is mainly expressed on the surface of innate immune cells.It can recognize pathogen related molecular patterns(PAMPs)or damage related molecular patterns(DAMPs).The innate immune system uses pattern recognition receptors to recognize pathogenic microorganisms in periodontal tissues and transmit signals to downstream pathways in time,thus triggering immune responses and then eliminating them.PRR has many family members,including toll like receptor family(TLRs),C-type lectin receptor family(CLRs),retinoic acid induced gene I(RIG-I)like receptor family(RLRs)and nucleotide binding oligomer domain(NOD)like receptor family(NLRs).Among them,RLRs are cytoplasmic receptors that recognize dsRNA from RNA viruses and have little association with chronic periodontitis.In this paper,the classification and structure of TLRs,CLRs,NLRs and the role of signal transduction pathway in chronic periodontitis are reviewed.In order to enrich the pathogenesis of periodontitis,provide new ideas for the treatment and prevention of chronic periodontitis.

Expression and clinical significance of pattern recognition receptor-associated genes in hand, foot and mouth disease

Objective:To explore which pattern recognition receptors(PRRs)play a key role in the development of hand,foot,and mouth disease(HFMD)by analyzing PRR-associated genes.Methods:We conducted a comparative analysis of PRR-associated gene expression in human peripheral blood mononuclear cells(PBMCs)infected with enterovirus 71(EV-A71)which were derived from patients with HFMD of different severities and at different stages.A total of 30 PRR-associated genes were identified as significantly upregulated both over time and across different EV-A71 isolates.Subsequently,ELISA was employed to quantify the expression of the six most prominent genes among these 30 identified genes,specifically,BST2,IRF7,IFI16,TRIM21,MX1,and DDX58.Results:Compared with those at the recovery stage,the expression levels of BST2(P=0.027),IFI16(P=0.016),MX1(P=0.046)and DDX58(P=0.008)in the acute stage of infection were significantly upregulated,while no significant difference in the expression levels of IRF7(P=0.495)and TRIM21(P=0.071)was found between different stages of the disease.The expression levels of BST2,IRF7,IFI16 and MX1 were significantly higher in children infected with single pathogen than those infected with mixed pathogens,and BST2,IRF7,IFI16 and MX1 expression levels were significantly lower in coxsackie B virus(COXB)positive patients than the negative patients.Expression levels of one or more of BST2,IRF7,IFI16,TRIM21,MX1 and DDX58 genes were correlated with PCT levels,various white blood cell counts,and serum antibody levels that reflect disease course of HFMD.Aspartate aminotransferase was correlated with BST2,MX1 and DDX58 expression levels.Conclusions:PRR-associated genes likely initiate the immune response in patients at the acute stage of HFMD.

Pattern recognition receptors in zebrafish provide functional and evolutionary insight into innate immune signaling pathways

Pattern recognition receptors （PRRs） and their signaling pathways have essential roles in recognizing various components of pathogens as well as damaged cells and triggering inflammatory responses that eliminate invading microorganisms and damaged cells. The zebrafish relies heavily on these primary defense mechanisms against pathogens. Here, we review the major PRR signaling pathways in the zebrafish innate immune system and compare these signaling pathways in zebrafish and humans to reveal their evolutionary relationship and better understand their innate immune defense mechanisms.

Expansion of pathogen recognition specificity in plants using pattern recognition receptors and artificially designed decoys

Pathogen/microbe-associated molecular patterns(PAMPs/MAMPs) are recognized by plant pattern recognition receptors(PRRs)localized on the cell surface to activate immune responses.This PAMP-triggered immunity(PTI) confers resistance to a broad range of pathogenic microbes and,therefore,has a great potential for genetically engineering broad-spectrum resistance by transferring PRRs across plant families.Pathogenic effectors secreted by phytopathogens often directly target and inhibit key components of PTI signaling pathways via diverse biochemical mechanisms.In some cases,plants have evolved to produce decoy proteins that mimic the direct virulence target,which senses the biochemical activities of pathogenic effectors.This kind of perception traps the effectors of erroneous targeting and results in the activation of effector-triggered immunity(ETI) instead of suppressing PTI.This mechanism suggests that artificially designed decoy proteins could be used to generate new recognition specificities in a particular plant.In this review,we summarize recent advances in research investigating PAMP recognition by PRRs and virulence effector surveillance by decoy proteins.Successful expansion of recognition specificities,conferred by the transgenic expression of EF-Tu receptor(EFR) and AvrPphB susceptible 1(PBS1) decoys,has highlighted the considerable potential of PRRs and artificially designed decoys to expand plant resistance spectra and the need to further identify novel PRRs and decoys.

Roles of pattern recognition receptors in diabetic nephropathy

Diabetic nephropathy(DN)is currently the most common complication of diabetes.It is considered to be one of the leading causes of end-stage renal disease(ESRD)and affects many diabetic patients.The pathogenesis of DN is extremely complex and has not yet been clarified;however,in recent years,increasing evidence has shown the important role of innate immunity in DN pathogenesis.Pattern recognition receptors(PRRs)are important components of the innate immune system and have a significant impact on the occurrence and development of DN.In this review,we classify PRRs into secretory,endocytic,and signal transduction PRRs according to the relationship between the PRRs and subcellular compartments.PRRs can recognize related pathogen-associated molecular patterns(PAMPs)and danger-associated molecular patterns(DAMPs),thus triggering a series of inflammatory responses,promoting renal fibrosis,and finally causing renal impairment.In this review,we describe the proposed role of each type of PRRs in the development and progression of DN.

Differential roles of RIG-Ⅰ like receptors in SARS-CoV-2 infection

Retinoic acid-inducible gene Ⅰ (RIG-Ⅰ) and melanoma differentiation-associated protein 5 (MDA5) sense viral RNA and activate antiviral immune responses.Herein we investigate their functions in human epithelial cells,the primary and initial target of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).A deficiency in MDA5,RIG-Ⅰ or mitochondrial antiviral signaling protein (MAVS) enhanced viral replication.The expression of the type I/III interferon(IFN) during infection was impaired in MDA5;and MAVS;,but not in RIG-Ⅰ;,when compared to wild type (WT) cells.The mRNA level of full-length angiotensin-converting enzyme 2 (ACE2),the cellular entry receptor for SARS-CoV-2,was approximately 2.5-fold higher in RIG-Ⅰ;than WT cells.These data demonstrate MDA5 as the predominant SARS-CoV-2 sensor,IFN-independent induction of ACE2 and anti-SARS-CoV-2 role of RIG-Ⅰ in epithelial cells.

Immune evasion strategies used by Helicobacter pylori

Helicobacter pylori(H. pylori) is perhaps the most ubiquitous and successful human pathogen, since it colonizes the stomach of more than half of humankind. Infection with this bacterium is commonly acquired during childhood. Once infected, people carry the bacteria for decades or even for life, if not treated. Persistent infection with this pathogen causes gastritis, peptic ulcer disease and is also strongly associated with the development of gastric cancer. Despite induction of innate and adaptive immune responses in the infected individual, the host is unable to clear the bacteria. One widely accepted hallmark of H. pylori is that it successfully and stealthily evades host defense mechanisms. Though the gastric mucosa is well protected against infection, H. pylori is able to reside under the mucus, attach to gastric epithelial cells and cause persistent infection by evading immune responses mediated by host. In this review, we discuss how H. pylori avoids innate and acquired immune response elements, uses gastric epithelial cells as mediators to manipulate host T cell responses and uses virulence factors to avoid adaptive immune responses by T cells to establish a persistent infection. We also discuss in this review how the genetic diversity of this pathogen helps for its survival.

Hepatitis B virus upregulates host expression of α-1,2-mannosidases via the PPARα pathway

AIM To assess the effects of hepatitis B virus(HBV) on the expression of host α-1,2-mannosidases and determine the underlying mechanisms.METHODS We measured the expression levels of MAN1A1, MAN1A2, MAN1B1, and MAN1C1 in cell lines HepG 2.2.15, HepN 10, HepA D38 and Hep G2 by Western blot. Viral antigens(HBs Ag and HBe Ag) in the culture medium were measured using the chemiluminescence method. HBV DNA quantification assays were performed using a commercial real-time PCR kit. Protein levels of human liver tissue α-1,2-mannosidases were also evaluated by Western blot. Plasmids containing seven individual viral genes of HBV(PTT22-HBx, PTT22-HBs, PTT22-pre S2, PTT22-pre S1, PTT22-HBc, PTT22-HBe, and PTT22-HBp) or control plasmids(PTT22-vector) were transfected into Hep G2 cells. MK886(PPARα) and GW9662(PPARγ) inhibitors were used to explore the effects of HBV on α-1,2-mannosidase expression after the PPARα and PPARγ pathways were blocked.RESULTS We showed that the expression of α-1,2-mannosidases was higher in stably transfected HBV cells than in controls. The expression levels of α-1,2-mannosidase were higher in AD38 cells than those in ND10 cells, which were in turn greater than those in G2.2.15 cells, and positively correlated with the expression of HBsA gin all the cell lines. Levels of α-1,2-mannosidase in nontumorous liver tissues of HBV-related HCC patients were also higher than in the tissues from non-HBVrelated HCC patients. Moreover, transfecting Hep G2 cells with a component of the HBV viral envelope also increased the expression of α-1,2-mannosidases. However, this envelope protein component could not induce MAN1C1 expression in the presence of a PPARα inhibitor, MK886. We also found that MK886 did not affect the expression of MAN1C1 in AD38 cells without tetracycline in the culture medium. This phenomenon was not observed in the case of GW9662.CONCLUSION Our results indicate that HBV increases the expression of α-mannosidases both in vitro and in vivo via activation of the PPARα pathway by its envelope protein.

Production of Transgenic Anliucheng Sweet Orange(Citrus sinensis Osbeck) with Xa21 Gene for Potential Canker Resistance

Citrus canker, an epidemic quarantine disease caused by Xanthomonas axonopodis pv. citri, has brought a great damage in citrus production worldwide. Herein, a rice PRR （pattern recognition receptor） gene Xa21 together with GUS reporter gene and hygromycin phosphotransferase gene （HPT） was introduced into Anliucheng sweet orange （Citrus sinensis Osbeck） via Agrobacterium-mediated transformation of embryogenic callus. The transgenic calluses were screened on MT basal medium containing hygromycin （HYG） and detected by histochemical GUS staining. The transgenic plantlets were recovered through somatic embryogenesis pathway. The regenerated plantlets were accustomed to and maintained in the greenhouse. The transgene integration of recovered plantlets was identiifed by PCR and Southern blot hybridization. It showed that all the transgenic plantlets tested had undergone single copy integration, the expression of Xa21 in eight different transgenic lines detected by qRT-PCR can be divided into three grades, high for T5 and T6, middle for T4 and low for the rest. The tolerance to citrus canker disease of the three recovered transgenic lines T2, T4 and T6 was assessed by in vitro pin-puncture inoculation. The results showed that all the three transgenic lines conferred improved resistance to citrus canker bacterium infection and the T4 transgenic line displayed the highest resistance. The mechanism and feasibility of rice Xa21 in triggering innate immunity in citrus was brielfy discussed.

Immunologic mechanism of fungal keratitis

Fungal keratitis(FK)is a refractory disease that poses a serious threat to vision,with common risk factors like eye trauma,contact lens wearing,topical corticosteroids and antibiotic abuse.Nowadays,topical and systemic anti-fungal drugs and ocular surgeries are still the main therapeutic modalities.However,the pathogenesis of FK,especially the immunologic mechanism within it,has not yet been deeply clarified.A better understanding of the pathogenesis of FK is imperative for more effective therapies and prognosis.Meanwhile,the immune protection strategies are also urgently required to manage FK.This review highlights recent advances in the immunologic mechanism in the pathogenesis of FK,in hope of providing valuable reference information for more effective anti-fungal treatment.

Functional identification of C-type lectin in the diamondback moth,Plutella xylostella(L.)innate immunity

C-type lectins(CTLs)are a superfamily of Ca^(2+)-dependent carbohydrate-recognition proteins,and an important pattern recognition receptor(PRR)in insect innate immunity which can mediate humoral and cellular immunity in insects.In this study,we report a novel dual carbohydrate-recognition domain(CRD)CTL from Plutella xylostella which we designate PxIML.PxIML is a protein with a 969 bp open reading frame(ORF)encoding 322 amino acids,containing a signal peptide and a dual-CRD with EPN(Glu_(124)-Pro_(125)-Asn_(126))and QPD(Gln_(274)-Pro_(275)-Asp_(276))motifs.The expression of PxIML mRNA in the fat body was significantly higher than in hemocytes and midgut.The relative expression levels of PxIML in the whole insect and the fat body were significantly inhibited after infection with Bacillus thuringiensis 8010(Bt8010)at 18 h,while they were significantly upregulated after infection with Serratia marcescens IAE6 or Pichia pastoris.The recombinant PxIML(rPxIML)protein could bind to the tested pathogen-associated molecular patterns(PAMPs),and the bacteria of Enterobacter sp.IAE5,S.marcescens IAE6,Staphylococcus aureus,Escherichia coli BL21,and Bt8010 in a Ca^(2+)-dependent manner,however,it showed limited binding to the fungus,P.pastoris.The rPxIML exhibited strong activity in the presence of Ca^(2+) to agglutinate Bt8010,Enterobacter sp.IAE5 and S.aureus,but it only weakly agglutinated with E.coli BL21,and could not agglutinate with S.marcescens IAE6 or P.pastoris.Furthermore,the rPxIML could bind to hemocytes,promote the adsorption of hemocytes to beads,and enhance the phenoloxidase(PO)activity and melanization of P.xylostella.Our results suggest that PxIML plays an important role in pathogen recognition and in mediating subsequent humoral and cellular immunity of P.xylostella.

Alterations of autophagic and innate immune responses by the Crohn’s disease-associated ATG16L1 mutation

Crohn’s disease(CD)is driven by the loss of tolerance to intestinal microbiota and excessive production of pro-inflammatory cytokines.These pro-inflammatory cytokines are produced by macrophages and dendritic cells(DCs)upon sensing the intestinal microbiota by the pattern recognition receptors(PRRs).Impaired activation of PRR-mediated signaling pathways is associated with chronic gastrointestinal inflammation,as shown by the fact that loss-of-function mutations in the nucleotide-binding oligomerization domain 2 gene increase the risk of CD development.Autophagy is an intracellular degradation process,during which cytoplasmic nutrients and intracellular pathogens are digested.Given that impaired reaction to intestinal microbiota alters signaling pathways mediated by PRRs,it is likely that dysfunction of the autophagic machinery is involved in the development of CD.Indeed,the loss-of-function mutation T300A in the autophagy related 16 like 1(ATG16L1)protein,a critical regulator of autophagy,increases susceptibility to CD.Recent studies have provided evidence that ATG16L1 is involved not only in autophagy,but also in PRR-mediated signaling pathways.ATG16L1 negatively regulates pro-inflammatory cytokine responses of macrophages and DCs after these cells sense the intestinal microbiota by PRRs.Here,we discuss the molecular mechanisms underlying the development of CD in the T300A ATG16L1 mutation by focusing on PRR-mediated signaling pathways.

Role of nucleic acid sensing in the pathogenesis of type 1 diabetes

During infections,nucleic acids of pathogens are also engaged in recognition via several exogenous and cytosolic pattern recognition receptors,such as the toll-like receptors,retinoic acid inducible gene-I-like receptors,and nucleotide-binding and oligomerization domain-like receptors.The binding of the pathogen-derived nucleic acids to their corresponding sensors initiates certain downstream signaling cascades culminating in the release of type-I interferons(IFNs),especially IFN-αand other cytokines to induce proinflammatory responses towards invading pathogens leading to their clearance from the host.Although these sensors are hardwired to recognize pathogen associated molecular patterns,like viral and bacterial nucleic acids,under unusual physiological conditions,such as excessive cellular stress and increased apoptosis,endogenous self-nucleic acids like DNA,RNA,and mitochondrial DNA are also released.The presence of these self-nucleic acids in extranuclear compartments or extracellular spaces or their association with certain proteins sometimes leads to the failure of discriminating mechanisms of nucleic acid sensors leading to proinflammatory responses as seen in autoimmune disorders,like systemic lupus erythematosus,psoriasis and to some extent in type 1 diabetes(T1D).This review discusses the involvement of various nucleic acid sensors in autoimmunity and discusses how aberrant recognition of self-nucleic acids by their sensors activates the innate immune responses during the pathogenesis of T1D.

The Role of CARD9 in Metabolic Diseases

Caspase recruitment domain containing protein 9(CARD9)is an adaptor protein that plays a critical role in pattern recognition receptors(PRRs)-mediated activation of NF-kB and mitogen-activated protein kinase(MAPK).This elicits initiation of the pro・inflammatory cytokines and leads to inflammatory responses,which has been recognized as a critical contributor to chronic inflammation.Current researches demonstrate that CARD9 is strongly associated with metabolic diseases,such as obesity,insulin resistance,atherosclerosis and so on.In this review,we summarize CARD9 signaling pathway and the role of CARD9 in metabolic diseases.

Cigarette smoking and innate immune responses to influenza infection

Cigarette smoking(CS) suppresses the immune system, and smoking is a well-known major risk factor for respiratory tract infections, including influenza infection. Both smoking cigarettes and passive smoking alter a wide range of immunological functions, including innate and adaptive immune responses. Past reviews on CS and innate immunity have been focused on the effects of CS on structural changes of the lung, as well as the effects on the function of alveolar macrophages, leukocytes, natural killer cells and dendritic cells. The study of innate immunity has developed rapidly in the last decade with the discovery of new receptors for virus recognition and interferon responses. This review aims to give a brief summary of recent findings on the suppressive effects of CS on the innate response to influenza virus, especially as it pertains to suppression of the function of pattern recognition receptors for influ-enza virus.

Identification of a novel C-type lectin from the shrimp Litopenaeus vannamei and its role in defense against pathogens infection

Acting as one of the pattern recognition receptors （PRRs）, C-type lectin is believed to mediate pathogen recognition and plays an important role in the clearance of pathogens as part of the innate immune system. In this work, a novel C-type lectin gene （named LvLecl） was cloned from the shrimp Litopenaeus vannamei, The ORF of LvLecl is 510 bp, encoding 169 amino acids. The deduced amino acid sequence contains a putative signal peptide of 19 amino acids at the N-terminal and a carbohydrate recognition domain （CRD） at the C-terminal. LvLecl was mainly expressed in the hepatopancreas. Real-time PCR analysis indicated that the level of LvLecl transcripts significantly changed in the hepatopancreas after the shrimp were artificially challenged with LPS, Micrococcus lysodeikticus and white spot syndrome virus （WSSV）. RNAi-based silencing of LvLecl resulted in increases in mortality when the shrimp were challenged with WSSV, and the median lethal time was reduced compared with controls. Although there was no characteristic ＂EPN＂ （Glu-Pro-Ser） or ＂QPD＂ （Gin-Pro-Asp） motif, the recombinant LvLecl, expressed in Escherichia coli BL21 （DE3）, could also agglutinate M. lysodeikticus and Vibrio anguillarum. The agglutinating activities were calcium-dependent and could be inhibited by D-mannose, D-glucose, D-galactose and N-Acetyl-D-mannose. These results suggest that LvLecl might be involved in the immune response against WSSV and bacterial infections and contribute to non-self recognition as a pattern recognition receptor in the innate immune system of the shrimp L. vannamei.

Plant cell wall-mediated disease resistance:Current understanding and future perspectives

Beyond their function as structural barriers,plant cell walls are essential elements for the adaptation of plants to environmental conditions.Cell walls are dynamic structures whose composition and integrity can be altered in response to environmental challenges and developmental cues.These wall changes are perceived by plant sensors/receptors to trigger adaptative responses during development and upon stress perception.Plant cell wall damage caused by pathogen infection,wounding,or other stresses leads to the release of wall molecules,such as carbohydrates(glycans),that function as damage-associated molecular patterns(DAMPs).DAMPs are perceived by the extracellular ectodomains(ECDs)of pattern recognition receptors(PRRs)to activate pattern-triggered immunity(PTI)and disease resistance.Similarly,glycans released from the walls and extracellular layers of microorganisms interacting with plants are recognized as microbe-associated molecular patterns(MAMPs)by specific ECD-PRRs triggering PTI responses.The number of oligosaccharides DAMPs/MAMPs identified that are perceived by plants has increased in recent years.However,the structural mechanisms underlying glycan recognition by plant PRRs remain limited.Currently,this knowledge is mainly focused on receptors of the LysM-PRR family,which are involved in the perception of various molecules,such as chitooligosaccharides from fungi and lipo-chitooligosaccharides(i.e.,Nod/MYC factors from bacteria and mycorrhiza,respectively)that trigger differential physiological responses.Nevertheless,additional families of plant PRRs have recently been implicated in oligosaccharide/polysaccharide recognition.These include receptor kinases(RKs)with leucine-rich repeat and Malectin domains in their ECDs(LRR-MAL RKs),Catharanthus roseus RECEPTOR-LIKE KINASE 1-LIKE group(CrRLK1L)with Malectin-like domains in their ECDs,as well as wall-associated kinases,lectin-RKs,and LRR-extensins.The characterization of structural basis of glycans recognition by these new plant receptors will shed light on their similarities with those of mammalians involved in glycan perception.The gained knowledge holds the potential to facilitate the development of sustainable,glycan-based crop protection solutions.

The macrophage soluble receptor AIM/Api6/CD5L displays a broad pathogen recognition spectrum and is involved in early response to microbial aggression

Apoptosis inhibitor of macrophages （AIMs）, a homologue of human Spa, is a mouse soluble member of the scavenger receptor cysteine-rich superfamily （SRCR-SF）. This family integrates a group of proteins expressed by innate and adaptive immune cells for which no unifying function has yet been described. Pleiotropic functions have been ascribed to AIM, from viability support in lymphocytes during thymic selection to lipid metabolism and anti-inflammatory effects in autoimmune pathologies. In the present report, the pathogen binding properties of AIM have been explored. By using a recombinant form of AIM （rAIM） expressed in mammalian cells, it is shown that this protein is able to bind and aggregate Gram-positive and Gram-negative bacteria, as well as pathogenic and saprophytic fungal species. Importantly, endogenous AIM from mouse serum also binds to microorganisms and secretion of AIM was rapidly induced in mouse spleen macrophages following exposure to conserved microbial cell wall components. Cytokine release induced by well-known bacterial and fungal Toll-like receptor （TLR） ligands on mouse splenocytes was also inhibited in the presence of rAIM. Furthermore, mouse models of pathogen-associated molecular patterns （PAMPs）-induced septic shock of bacterial and fungal origin showed that serum AIM levels changed in a time-dependent manner. Altogether, these data suggest that AIM plays a general homeostatic role by supporting innate humoral defense during pathogen aggression.

Microbial sensing in the intestine

The gut microbiota plays a key role in host health and disease,particularly through their interactions with the immune system.Intestinal homeostasis is dependent on the symbiotic relationships between the host and the diverse gut microbiota,which is influenced by the highly co-evolved immune-microbiota interactions.The first step of the interaction between the host and the gut microbiota is the sensing of the gut microbes by the host immune system.In this review,we describe the cells of the host immune system and the proteins that sense the components and metabolites of the gut microbes.We further highlight the essential roles of pattern recognition receptors(PRRs),the G protein-coupled receptors(GPCRs),aryl hydrocarbon receptor(AHR)and the nuclear receptors expressed in the intestinal epithelial cells(IECs)and the intestine-resident immune cells.We also discuss the mechanisms by which the disruption of microbial sensing because of genetic or environmental factors causes human diseases such as the inflammatory bowel disease(IBD).

Expression of Innate Immunity Genes in Epithelial Cells of Hypertrophic Adenoids with and without Pediatric Chronic Rhinosinusitis： A Preliminary Report

Background： Adenoid hypertrophy （AH） is associated with pediatric chronic rhinosinusitis （pCRS）, but its role in the inflammatory process of pCRS is unclear. It is thought that innate immunity gene expression is disrupted in the epithelium of patients with chronic rhinosinusitis （CRS）, including antimicrobial peptides and pattern recognition receptors （PRRs）. The aim of this preliminary study was to detect the expression of innate immunity genes in epithelial cells of hypertrophic adenoids with and without pCRS to better understand their role in pCRS. Methods： Nine pCRS patients and nine simple AH patients undergoing adenoidectomy were recruited for the study. Adenoidal epithelium was isolated, and real-time quantitative polymerase chain reaction （RT-qPCR） was employed to measure relative expression levels of the following messenger RNAs in hypertrophic adenoid epithelial cells of pediatric patients with and without CRS： Human β-defensin （HBD） 2 and 3, surfactant protein （SP）-A and D, toll-like receptors 1-10, nucleotide-binding oligomerization domain （NOD）-like receptors NOD 1, NOD 2, and NACHT, LRR and PYD domains-containing protein 3, retinoic acid-induced gene 1, melanoma differentiation-associated gene 5, and nuclear factor-riB （NF-KB）. RT-qPCR data from two groups were analyzed by independent sample t-tests and Mann-Whitney U-tests. Results： The relative expression of SP-D in adenoidal epithelium ofpCRS group was significantly lower than that in AH group （pCRS 0.73 ± 0.10 vs. AH 1.21 ±0.15; P = 0.0173, t = 2.654）. The relative expression levels of all tested PRRs and NF-κB, as well as HBD-2, HBD-3, and SP-A, showed no statistically significant differences in isolated adenoidal epithelium between pCRS group and AH group. Conclusions： Down-regulated SP-D levels in adenoidal epithelium may contribute to the development of pCRS. PRRs, however, are unlikely to play a significant role in the inflammatory process ofpCRS.