@article{Mutavhatsindi2022a,
abstract = {Objectives: To better understand the pathogenesis of pericardial tuberculosis (PCTB), we sought to characterize the systemic inflammatory profile in HIV-1-infected participants with latent TB infection (LTBI), pulmonary TB (PTB) and PCTB. Methods: Using Luminex, we measured 39 analytes in pericardial fluid (PCF) and paired plasma from 18 PCTB participants, and plasma from 16 LTBI and 20 PTB. Follow-up plasma samples were also obtained from PTB and PCTB participants. HLA-DR expression on Mtb-specific CD4 T cells was measured in baseline samples using flow cytometry. Results: Assessment of the overall systemic inflammatory profile by principal component analysis showed that the inflammatory profile of active TB participants was distinct from the LTBI group, while PTB patients could not be distinguished from those with PCTB. In the LTBI group, 12 analytes showed a positive association with plasma HIV-1 viral load, and most of these associations were lost in the diseased groups. When comparing the inflammatory profile between PCF and paired blood, we found that the concentrations of most analytes (24/39) were elevated at site of disease. However, the inflammatory profile in PCF partially mirrored inflammatory events in the blood. After TB treatment completion, the overall plasma inflammatory profile reverted to those observed in the LTBI group. Lastly, HLA-DR expression showed the best performance for TB diagnosis compared to previously described biosignatures built from soluble markers. Conclusion: Our results describe the inflammatory profile associated with PTB and PCTB and emphasize the potential role of HLA-DR as a promising biomarker for TB diagnosis. {\#}{\#}{\#} Competing Interest Statement The authors have declared no competing interest.},
author = {Mutavhatsindi, Hygon and Bruyn, Elsa Du and Ruzive, Sheena and Howlett, Patrick and Sher, Alan and Mayer-Barber, Katrin D and Barber, Daniel L and Ntsekhe, Mpiko and Wilkinson, Robert J and Riou, Catherine},
doi = {10.1101/2022.10.21.513232},
file = {:C$\backslash$:/Users/01462563/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Mutavhatsindi et al. - 2022 - Blood and site of disease inflammatory profiles differ in HIV-1-infected pericardial tuberculosis patients.pdf:pdf},
journal = {bioRxiv},
keywords = {51,Inflammatory profile,OA,Pericardial tuberculosis,diagnosis,fund{\_}ack,original,site of disease},
mendeley-tags = {OA,fund{\_}ack,original},
month = {oct},
pages = {2022.10.21.513232},
publisher = {Cold Spring Harbor Laboratory},
title = {{Blood and site of disease inflammatory profiles differ in HIV-1-infected pericardial tuberculosis patients}},
url = {https://www.biorxiv.org/content/10.1101/2022.10.21.513232v1 https://www.biorxiv.org/content/10.1101/2022.10.21.513232v1.abstract},
year = {2022}
}

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HLA-DR expression on Mtb-specific CD4 T cells was measured in baseline samples using flow cytometry. Results: Assessment of the overall systemic inflammatory profile by principal component analysis showed that the inflammatory profile of active TB participants was distinct from the LTBI group, while PTB patients could not be distinguished from those with PCTB. In the LTBI group, 12 analytes showed a positive association with plasma HIV-1 viral load, and most of these associations were lost in the diseased groups. When comparing the inflammatory profile between PCF and paired blood, we found that the concentrations of most analytes (24/39) were elevated at site of disease. However, the inflammatory profile in PCF partially mirrored inflammatory events in the blood. After TB treatment completion, the overall plasma inflammatory profile reverted to those observed in the LTBI group. Lastly, HLA-DR expression showed the best performance for TB diagnosis compared to previously described biosignatures built from soluble markers. Conclusion: Our results describe the inflammatory profile associated with PTB and PCTB and emphasize the potential role of HLA-DR as a promising biomarker for TB diagnosis. ### Competing Interest Statement The authors have declared no competing interest.","author":[{"propositions":[],"lastnames":["Mutavhatsindi"],"firstnames":["Hygon"],"suffixes":[]},{"propositions":[],"lastnames":["Bruyn"],"firstnames":["Elsa","Du"],"suffixes":[]},{"propositions":[],"lastnames":["Ruzive"],"firstnames":["Sheena"],"suffixes":[]},{"propositions":[],"lastnames":["Howlett"],"firstnames":["Patrick"],"suffixes":[]},{"propositions":[],"lastnames":["Sher"],"firstnames":["Alan"],"suffixes":[]},{"propositions":[],"lastnames":["Mayer-Barber"],"firstnames":["Katrin","D"],"suffixes":[]},{"propositions":[],"lastnames":["Barber"],"firstnames":["Daniel","L"],"suffixes":[]},{"propositions":[],"lastnames":["Ntsekhe"],"firstnames":["Mpiko"],"suffixes":[]},{"propositions":[],"lastnames":["Wilkinson"],"firstnames":["Robert","J"],"suffixes":[]},{"propositions":[],"lastnames":["Riou"],"firstnames":["Catherine"],"suffixes":[]}],"doi":"10.1101/2022.10.21.513232","file":":C$\\$:/Users/01462563/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Mutavhatsindi et al. - 2022 - Blood and site of disease inflammatory profiles differ in HIV-1-infected pericardial tuberculosis patients.pdf:pdf","journal":"bioRxiv","keywords":"51,Inflammatory profile,OA,Pericardial tuberculosis,diagnosis,fund_ack,original,site of disease","mendeley-tags":"OA,fund_ack,original","month":"oct","pages":"2022.10.21.513232","publisher":"Cold Spring Harbor Laboratory","title":"Blood and site of disease inflammatory profiles differ in HIV-1-infected pericardial tuberculosis patients","url":"https://www.biorxiv.org/content/10.1101/2022.10.21.513232v1 https://www.biorxiv.org/content/10.1101/2022.10.21.513232v1.abstract","year":"2022","bibtex":"@article{Mutavhatsindi2022a,\r\nabstract = {Objectives: To better understand the pathogenesis of pericardial tuberculosis (PCTB), we sought to characterize the systemic inflammatory profile in HIV-1-infected participants with latent TB infection (LTBI), pulmonary TB (PTB) and PCTB. Methods: Using Luminex, we measured 39 analytes in pericardial fluid (PCF) and paired plasma from 18 PCTB participants, and plasma from 16 LTBI and 20 PTB. Follow-up plasma samples were also obtained from PTB and PCTB participants. HLA-DR expression on Mtb-specific CD4 T cells was measured in baseline samples using flow cytometry. Results: Assessment of the overall systemic inflammatory profile by principal component analysis showed that the inflammatory profile of active TB participants was distinct from the LTBI group, while PTB patients could not be distinguished from those with PCTB. In the LTBI group, 12 analytes showed a positive association with plasma HIV-1 viral load, and most of these associations were lost in the diseased groups. When comparing the inflammatory profile between PCF and paired blood, we found that the concentrations of most analytes (24/39) were elevated at site of disease. However, the inflammatory profile in PCF partially mirrored inflammatory events in the blood. After TB treatment completion, the overall plasma inflammatory profile reverted to those observed in the LTBI group. Lastly, HLA-DR expression showed the best performance for TB diagnosis compared to previously described biosignatures built from soluble markers. 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