Alteration of Polymeric Immunoglobulin Receptor and Neonatal Fc Receptor Expression in the Gut Mucosa of Immunodeficiency Virus‐Infected Rhesus Macaques

Wang, Y; Yang, Guan‐Wen

doi:10.1111/sji.12416

Cited by 12 publications

(5 citation statements)

References 64 publications

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“…When the pathogen stimulates the mucosal epithelium, the expression of FcRn may be regulated. Simian/human immunodeficiency virus (SHIV) infection decreases FcRn and pIgR expression, which may also be the mechanism responsible for its pathogenesis in rhesus monkeys (Wang and Yang, 2016). On the other hand, TGEV up-regulates FcRn expression, which is potentially what provides the mucosal protection.…”

Section: Discussionmentioning

confidence: 99%

Transmissible Gastroenteritis Virus Infection Up-Regulates FcRn Expression via Nucleocapsid Protein and Secretion of TGF-β in Porcine Intestinal Epithelial Cells

et al. 2020

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Transmissible gastroenteritis virus (TGEV) is a porcine intestinal coronavirus that causes fatal severe watery diarrhea in piglets. The neonatal Fc receptor (FcRn) is the only IgG transport receptor, its expression on mucosal surfaces is triggered upon viral stimulation, which significantly enhances mucosal immunity. We utilized TGEV as a model pathogen to explore the role of FcRn in resisting viral invasion in overall intestinal mucosal immunity. TGEV induced FcRn expression by activating NF-κB signaling in porcine small intestinal epithelial (IPEC-J2) cells, however, the underlying mechanisms are unclear. First, using small interfering RNAs, we found that TGEV up-regulated FcRn expression via TLR3, TLR9 and RIG-I. Moreover, TGEV induced IL-1β, IL-6, IL-8, TGF-β, and TNF-α production. TGF-β-stimulated IPEC-J2 cells highly up-regulated FcRn expression, while treatment with a JNK-specific inhibitor down-regulated the expression. TGEV nucleocapsid (N) protein also enhanced FcRn promoter activity via the NF-κB signaling pathway and its central region (aa 128-252) was essential for FcRn activation. Additionally, N protein-mediated FcRn up-regulation promotes IgG transcytosis. Thus, TGEV N protein and TGF-β up-regulated FcRn expression, further clarifying the molecular mechanism of up-regulation of FcRn expression by TGEV.

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Section: Discussionmentioning

confidence: 99%

Transmissible Gastroenteritis Virus Infection Up-Regulates FcRn Expression via Nucleocapsid Protein and Secretion of TGF-β in Porcine Intestinal Epithelial Cells

et al. 2020

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“…However, recent studies have found that IgG also plays an important role against pathogen infection in mucosal sites, while the neonatal Fc receptor (FcRn) is the only IgG transport receptor (Tsuruta et al, 2012). Down-regulation of FcRn and pIgR has been shown in the tracheal mucosa of SHIV/SIV-infected rhesus macaques (Wang and Yang, 2016; Li et al, 2017). Further, transmissible gastroenteritis virus infection up-regulates FcRn through TLR3 and RIG-I in porcine intestinal epithelial cells (unpublished results).…”

Section: Discussionmentioning

confidence: 99%

Isolation and Identification of Porcine Epidemic Diarrhea Virus and Its Effect on Host Natural Immune Response

et al. 2019

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Porcine epidemic diarrhea (PED) is a highly infectious intestinal disease caused by porcine epidemic diarrhea virus (PEDV). A PEDV strain was isolated from the piglet intestinal tract in Vero cells in Jiangsu Province, designated as the JS-A strain. PEDV was identified as the isolated virus by cytopathology, immunofluorescence assay, western blotting, transmission electron microscopy, and sequence analysis. The full-length genome of the JS-A isolate and the S gene were systematically analyzed, indicating that PEDV JS-A belongs to the G2a subtype, which is closely related to the prevalent PEDV in many countries and different from many current vaccines. Animal regression tests showed that piglets that are orally infected with the virus continue to develop diarrhea with yellowish and unpleasant odors. Further, piglets showed reduced food consumption and weight loss in the challenged group, while there were no abnormalities in the control group. In addition, Toll-like receptors (TLRs), RIG-I, and the downstream medium gene in the intestinal mucosa of newborn pigs infected with PEDV JS-A strain were studied. The neonatal Fc receptor (FcRn) was the only IgG transport receptor and protected IgG from degradation. Therefore, PEDV JS-A infection might inhibit FcRn expression by down-regulating TLRs and downstream signaling molecules. Taken together, isolation of the JS-A variant contributes to evolutionary analysis of the diarrhea virus. Further, the experimental infection model lays a foundation for further research related to vaccine development and the antiviral natural immune response of infected piglets, which helps us to better understand PEDV pathogenesis and immune mechanism.

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“…For example, enterotoxigenic E. coli suppresses pIgR mRNA expression in vivo [ 118 ]. Similarly, simian immunodeficiency virus (SIV) and chimeric simian/human immunodeficiency virus (S/HIV) was able to downregulate pIgR mRNA expression in the gastrointestinal and respiratory mucosa of infected rhesus macaques [ 119 , 120 ], suggesting HIV may also use pIgR downregulation as an immune evasion tactic.…”

Section: Subversion Of the Pigr/sig System By Pathogensmentioning

confidence: 99%

The Role of the Polymeric Immunoglobulin Receptor and Secretory Immunoglobulins during Mucosal Infection and Immunity

Turula

Wobus

2018

Viruses

133

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The gastrointestinal tract houses millions of microbes, and thus has evolved several host defense mechanisms to keep them at bay, and prevent their entry into the host. One such mucosal surface defense is the secretion of secretory immunoglobulins (SIg). Secretion of SIg depends on the polymeric immunoglobulin receptor (pIgR), which transports polymeric Ig (IgA or IgM) from the basolateral surface of the epithelium to the apical side. Upon reaching the luminal side, a portion of pIgR, called secretory component (SC) is cleaved off to release Ig, forming SIg. Through antigen-specific and non-specific binding, SIg can modulate microbial communities and pathogenic microbes via several mechanisms: agglutination and exclusion from the epithelial surface, neutralization, or via host immunity and complement activation. Given the crucial role of SIg as a microbial scavenger, some pathogens also evolved ways to modulate and utilize pIgR and SIg to facilitate infection. This review will cover the regulation of the pIgR/SIg cycle, mechanisms of SIg-mediated mucosal protection as well as pathogen utilization of SIg.

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Alteration of Polymeric Immunoglobulin Receptor and Neonatal Fc Receptor Expression in the Gut Mucosa of Immunodeficiency Virus‐Infected Rhesus Macaques

Cited by 12 publications

References 64 publications

Transmissible Gastroenteritis Virus Infection Up-Regulates FcRn Expression via Nucleocapsid Protein and Secretion of TGF-β in Porcine Intestinal Epithelial Cells

Transmissible Gastroenteritis Virus Infection Up-Regulates FcRn Expression via Nucleocapsid Protein and Secretion of TGF-β in Porcine Intestinal Epithelial Cells

Isolation and Identification of Porcine Epidemic Diarrhea Virus and Its Effect on Host Natural Immune Response

The Role of the Polymeric Immunoglobulin Receptor and Secretory Immunoglobulins during Mucosal Infection and Immunity

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