Back

HIV Infection impairs the Host Response to Mycobacterium tuberculosis Infection by altering Surfactant Protein D function in the Human Lung Alveolar Mucosa

Akhter, A.; Moliva, J.; Azad, A. K.; Olmo-Fontanez, A. M.; Garcia-Vilanova, A.; Scordo, J. M.; Gavrilin, M.; Diaz, P.; Endsley, J.; Weintraub, S.; Schlesinger, L.; Wewers, M.; Torrelles, J. B.

2023-10-01 cell biology
10.1101/2023.10.01.560171 bioRxiv
Show abstract

Tuberculosis is the leading cause of death for people living with HIV (PLWH). We hypothesized that altered functions of innate immune components in the human alveolar lining fluid of PLWH (HIV-ALF), drive susceptibility to Mycobacterium tuberculosis (M.tb) infection. Our results indicate a significant increase in oxidation of innate proteins and chemokine levels, and significantly lower levels and function of complement components and Th1/Th2/Th17 cytokines in HIV-ALF vs. control-ALF (non-HIV infected people). We further found a deficiency of surfactant protein-D (SP-D) and reduced binding of SP-D to M.tb that had been exposed to HIV-ALF. Primary human macrophages infected with M.tb exposed to HIV-ALF were significantly less capable of controlling the infection, which was reversed by SP-D replenishment in HIV-ALF. Thus, our data suggest that PLWH without antiretroviral therapy (ART) have declining host innate defense function in their lung mucosa, thereby favoring M.tb and potentially other pulmonary infections.

Matching journals

The top 8 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.