Role of Humoral Immunity in Whole-Cell Vaccine-Mediated Protection against Pseudomonas aeruginosa
Pseudomonas aeruginosa can cause a wide range of multidrug-resistant infections. However, there is currently no licensed P. aeruginosa vaccine. Understanding the required immune response to confer protection can help develop future vaccines and therapeutics against this bacterium. Sen-Kilic et al. (e00451-20) characterize mechanistic correlates of protection provided by whole-cell vaccination against P. aeruginosa during infection. Their data indicate that B cells and antibodies play a crucial role in whole-cell vaccine-induced protection against P. aeruginosa. In particular, their findings suggest that T cell-independent antibody production induced by whole-cell vaccination is sufficient for bacterial clearance during acute lung pneumonia.
Cholera Toxin Activates the Unfolded Protein Response To Enhance Intoxication
The profuse watery diarrhea of cholera results from a G protein-dependent signaling event that involves adenylate cyclase and elevated levels of cAMP. This process begins when cholera toxin reaches the host cytosol and activates the heterotrimeric G protein. Banerjee et al. (e00447-20) found that the activated G protein also triggers the unfolded protein response (UPR) by an atypical mechanism that does not involve the adenylate cyclase/cAMP signaling pathway. UPR activation enhanced toxin delivery to the cytosol, thus producing a toxin-sensitive phenotype. These results indicate that there is a cAMP-independent response to cholera toxin that triggers the UPR and enhances the efficiency of intoxication.
Role of CXCR3 during Pregnancy in Toxoplasma Infection
Symptoms of congenital toxoplasmosis range from embryonic death and resorption to subclinical infection, but the role of chemokine receptor for disease onset remains unclear. This study (e00253-20) shows that C-X-C motif chemokine receptor 3 (CXCR3)-dependent immune responses provided anti-Toxoplasma activity and play an essential role in reducing embryo resorption and fetal loss caused by T. gondii infection during early pregnancy. The present results will contribute to explore a new potential therapeutic approach for protection against T. gondii infection during early pregnancy.
Staying Neutral on Vaginal pH
An indispensable murine model has been extensively utilized to delineate both fungal and host immune mechanisms that contribute to the pathogenesis of vulvovaginal candidiasis (VVC). Despite general acceptance that murine vaginal pH is neutral and differs from acidic pH observed in women, studies have failed to explicitly demonstrate this in the context of VVC. Using a combination of phenol red measurements and a pH-sensitive fungal reporter strain, Miao et al. (e00550-20) conclusively show that the murine global vaginal pH remains neutral, independent of fungal colonization, mouse strain, or hormonal regulation. Thus, contributions of vaginal pH to VVC symptomatology is further questioned.
- Copyright © 2021 American Society for Microbiology.
