Modulation of the immune response to Mycobacterium tuberculosis during malaria/M. tuberculosis co-infection

Tuberculosis (TB) causes significant morbidity and mortality on a global scale. The African region has 24% of the world's TB cases. TB overlaps with other infectious diseases such as malaria and HIV, which are also highly prevalent in the African region. TB is a leading cause of death among HIV-positive patients and co-infection with HIV and TB has been described as a syndemic. In view of the overlapping epidemiology of these diseases, it is important to understand the dynamics of the immune response to TB in the context of co-infection. We investigated the cytokine response to purified protein derivative (PPD) in peripheral blood mononuclear cells from TB patients co-infected with HIV or malaria and compared it to that of malaria- and HIV-free TB patients. A total of 231 subjects were recruited for this study and classified into six groups; untreated TB-positive, TB positive subjects on TB drugs, TB- and HIV-positive, TB- and malaria-positive, latent TB and apparently healthy control subjects. Our results demonstrate maintenance of interferon (IFN)-γ production in HIV and malaria co-infected TB patients in spite of lower CD4 counts in the HIV-infected cohort. Malaria co-infection caused an increase in the production of the T helper type 2 (Th2)-associated cytokine interleukin (IL)-4 and the anti-inflammatory cytokine IL-10 in PPD-stimulated cultures. These results suggest that malaria co-infection diverts immune response against M. tuberculosis towards a Th-2/anti-inflammatory response which might have important consequences for disease progression

Sequence Analysis Reveals Asymptomatic Infection with Mycoplasma Hominis and Ureaplasma Urealyticum Possibly Leads to Infertility in Females: A Cross-sectional Study

Background: Genetic evidence of asymptomatic Mycoplasma hominis (M. hominis) and Ureaplasma urealyticum (U. urealyticum) infection associated with infertility among females is lacking because suitable high throughput molecular methods have not been applied. Objective: This study aimed to explore the occurrence of M. hominis and U. urealyticum in the genital tract of females with asymptomatic infection and infertility as well as determine their genetic relatedness. Materials and Methods: The study group included 100 asymptomatic females and 31 females diagnosed with infertility. Sequencing of the 16S rRNA gene following DNA extraction was performed directly from endo-cervical swabs. Phylogenetic analysis established the genetic linkage between the isolates from both groups. Results: In asymptomatic females, M. hominis and U. urealyticum were detected with a prevalence of 8% and 2% respectively. Among females with infertility, the prevalence was 6.45% and 3.23% for M. hominis and U. urealyticum respectively. In both groups, M. hominis occurred significantly more frequently. Phylogenetic analysis revealed three distinct clusters in both groups: two with already characterized M. hominis and Ureaplasma species (28.6% of the overall Mycoplasma spp.) and one distinct cluster matched with U. urealyticum. Furthermore, all M. hominis from asymptomatic females clustered significantly with infertility contrary to U. urealyticum. The M. hominis cluster was significantly linked to two strains from China. Conclusion: The sequence analysis of Mycoplasma and Ureaplasma in the genital tract of asymptomatic and infertile females showed significant association; therefore, it is paramount to consider them as possible etiologic agents of infertility and genital infection, especially when the etiology of infertility is unknown. Key words: Mycoplasma hominis, Ureaplasma urealyticum, Genetic linkage, Asymptomatic infections, Infertility

Modulation of the immune response to Mycobacterium tuberculosis during malaria/M. tuberculosis co-infection

Tuberculosis (TB) causes significant morbidity and mortality on a global scale. The African region has 24% of the world's TB cases. TB overlaps with other infectious diseases such as malaria and HIV, which are also highly prevalent in the African region. TB is a leading cause of death among HIV-positive patients and co-infection with HIV and TB has been described as a syndemic. In view of the overlapping epidemiology of these diseases, it is important to understand the dynamics of the immune response to TB in the context of co-infection. We investigated the cytokine response to purified protein derivative (PPD) in peripheral blood mononuclear cells from TB patients co-infected with HIV or malaria and compared it to that of malaria- and HIV-free TB patients. A total of 231 subjects were recruited for this study and classified into six groups; untreated TB-positive, TB positive subjects on TB drugs, TB- and HIV-positive, TB- and malaria-positive, latent TB and apparently healthy control subjects. Our results demonstrate maintenance of interferon (IFN)-γ production in HIV and malaria co-infected TB patients in spite of lower CD4 counts in the HIV-infected cohort. Malaria co-infection caused an increase in the production of the T helper type 2 (Th2)-associated cytokine interleukin (IL)-4 and the anti-inflammatory cytokine IL-10 in PPD-stimulated cultures. These results suggest that malaria co-infection diverts immune response against M. tuberculosis towards a Th-2/anti-inflammatory response which might have important consequences for disease progression