Shilpa Naik1,2, Mallika Alexander1, Pavan Kumar3, Vandana Kulkarni1, Prasad Deshpande1, Su Yadana4, Cheng-Shiun Leu5, Mariana Araújo-Pereira6,7,8, Bruno B Andrade6,7,8,9,10,11, Ramesh Bhosale1,2, Subash Babu3, Amita Gupta1,12, Jyoti S Mathad13, Rupak Shivakoti4. 1. Byramjee-Jeejeebhoy Government Medical College-Johns Hopkins University Clinical Research Site, Pune, India. 2. Department of Obstetrics and Gynecology, Byramjee Jeejeebhoy Government Medical College, Pune, India. 3. International Center for Excellence in Research, National Institutes of Health, National Institute for Research in Tuberculosis, Chennai, India. 4. Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, United States. 5. Department of Biostatistics, Columbia University Mailman School of Public Health, New York, NY, United States. 6. Instituto Goncalo Moniz, Fundação Oswaldo Cruz, Salvador, Brazil. 7. Multinational Organization Network Sponsoring Translational and Epidemiological Research, Fundação José Silveira, New York, NY, Brazil. 8. Faculdade de Medicina, Universidade Federal da Bahia, Salvador, Brazil. 9. Curso de Medicina, Faculdade de Tecnologia e Ciências, Salvador, Brazil. 10. Escola de Medicina, Universidade Salvador (UNIFACS), Laureate International Universities, Salvador, Brazil. 11. Curso de Medicina, Escola Bahiana de Medicina e Saúde Pública (EBMSP), Salvador, Brazil. 12. Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States. 13. Department of Medicine, Weill Cornell Medical College, New York, NY, United States.
Abstract
Background: Recent studies in adults have characterized differences in systemic inflammation between adults with and without latent tuberculosis infection (LTBI+ vs. LTBI-). Potential differences in systemic inflammation by LTBI status has not been assess in pregnant women. Methods: We conducted a cohort study of 155 LTBI+ and 65 LTBI- pregnant women, stratified by HIV status, attending an antenatal clinic in Pune, India. LTBI status was assessed by interferon gamma release assay. Plasma was used to measure systemic inflammation markers using immunoassays: IFNβ, CRP, AGP, I-FABP, IFNγ, IL-1β, soluble CD14 (sCD14), sCD163, TNF, IL-6, IL-17a and IL-13. Linear regression models were fit to test the association of LTBI status with each inflammation marker. We also conducted an exploratory analysis using logistic regression to test the association of inflammatory markers with TB progression. Results: Study population was a median age of 23 (Interquartile range: 21-27), 28% undernourished (mid-upper arm circumference (MUAC) <23 cm), 12% were vegetarian, 10% with gestational diabetes and 32% with HIV. In multivariable models, LTBI+ women had significantly lower levels of third trimester AGP, IL1β, sCD163, IL-6 and IL-17a. Interestingly, in exploratory analysis, LTBI+ TB progressors had significantly higher levels of IL1β, IL-6 and IL-13 in multivariable models compared to LTBI+ non-progressors. Conclusions: Our data shows a distinct systemic immune profile in LTBI+ pregnant women compared to LTBI- women. Data from our exploratory analysis suggest that LTBI+ TB progressors do not have this immune profile, suggesting negative association of this profile with TB progression. If other studies confirm these differences by LTBI status and show a causal relationship with TB progression, this immune profile could identify subsets of LTBI+ pregnant women at high risk for TB progression and who can be targeted for preventative therapy.
Background: Recent studies in adults have characterized differences in systemic inflammation between adults with and without latent tuberculosis infection (LTBI+ vs. LTBI-). Potential differences in systemic inflammation by LTBI status has not been assess in pregnant women. Methods: We conducted a cohort study of 155 LTBI+ and 65 LTBI- pregnant women, stratified by HIV status, attending an antenatal clinic in Pune, India. LTBI status was assessed by interferon gamma release assay. Plasma was used to measure systemic inflammation markers using immunoassays: IFNβ, CRP, AGP, I-FABP, IFNγ, IL-1β, soluble CD14 (sCD14), sCD163, TNF, IL-6, IL-17a and IL-13. Linear regression models were fit to test the association of LTBI status with each inflammation marker. We also conducted an exploratory analysis using logistic regression to test the association of inflammatory markers with TB progression. Results: Study population was a median age of 23 (Interquartile range: 21-27), 28% undernourished (mid-upper arm circumference (MUAC) <23 cm), 12% were vegetarian, 10% with gestational diabetes and 32% with HIV. In multivariable models, LTBI+ women had significantly lower levels of third trimester AGP, IL1β, sCD163, IL-6 and IL-17a. Interestingly, in exploratory analysis, LTBI+ TB progressors had significantly higher levels of IL1β, IL-6 and IL-13 in multivariable models compared to LTBI+ non-progressors. Conclusions: Our data shows a distinct systemic immune profile in LTBI+ pregnant women compared to LTBI- women. Data from our exploratory analysis suggest that LTBI+ TB progressors do not have this immune profile, suggesting negative association of this profile with TB progression. If other studies confirm these differences by LTBI status and show a causal relationship with TB progression, this immune profile could identify subsets of LTBI+ pregnant women at high risk for TB progression and who can be targeted for preventative therapy.
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