Expression of pIgR in the tracheal mucosa of SHIV/SIV-infected rhesus macaques

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Polymeric immunoglobulin receptors(pIgR) are key participants in the formation and secretion of secretory Ig A(S-Ig A), which is critical for the prevention of microbial infection and colonization in the respiratory system. Although increased respiratory colonization and infections are common in HIV/AIDS, little is known about the expression of pIgR in the airway mucosa of these patients. To address this, the expression levels of pIgR in the tracheal mucosa and lungs of SHIV/SIV-infected rhesus macaques were examined by real-time RTPCR and confocal microscopy. We found that the levels of both PIGR m RNA and pIgR immunoreactivity were lower in the tracheal mucosa of SHIV/SIVinfected rhesus macaques than that in non-infected rhesus macaques, and the difference in pIgR immunoreactivity was statistically significant. IL-17 A, which enhances pIgR expression, was also changed in the same direction as that of pIgR. In contrast to changes in the tracheal mucosa, pIgR and IL-17 A levels were higher in the lungs of infected rhesus macaques. These results indicated abnormal pIgR expression in SHIV/SIV, and by extension HIV infections, which might partially result from IL-17 A alterations and might contribute to the increased microbial colonization and infection related to pulmonary complications in HIV/AIDS. Polymeric immunoglobulin receptors (pIgR) are key participants in the formation and secretion of secretory Ig A (S-Ig A), which is critical for the prevention of microbial infection and colonization in the respiratory system. To address this, the expression levels of pIgR in the tracheal mucosa and lungs of SHIV / SIV-infected rhesus macaques were examined by real-time RTPCR We found that the levels of both PIGR m RNA and pIgR immunoreactivity were lower in the tracheal mucosa of SHIV / SIVinfected rhesus macaques than that in non-infected rhesus macaques, and the difference in pIgR immunoreactivity was significantly. IL- 17 A, which enhances pIgR expression, was also changed in the same direction as that of pIgR. In contrast to changes in the tracheal mucosa, plgR and IL-17 A levels were hi gher in the lungs of infected rhesus macaques. These results indicate abnormal pIgR expression in SHIV / SIV, and by extension HIV infections, which by partially result from IL-17 A alterations and may contribute to the increased microbial colonization and infection related to pulmonary complications in HIV / AIDS.
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