Biofilm formation in the lung contributes to virulence and drug tolerance of Mycobacterium tuberculosis

Poushali Chakraborty, Sapna Bajeli, Deepak Kaushal, Bishan Dass Radotra and Ashwani Kumar ()
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Poushali Chakraborty: Council of Scientific and Industrial Research, Institute of Microbial Technology
Sapna Bajeli: Council of Scientific and Industrial Research, Institute of Microbial Technology
Deepak Kaushal: Southwest National Primate Research Center, Texas Biomedical Research Institute
Bishan Dass Radotra: Postgraduate Institute of Medical Education and Research
Ashwani Kumar: Council of Scientific and Industrial Research, Institute of Microbial Technology

Nature Communications, 2021, vol. 12, issue 1, 1-17

Abstract: Abstract Tuberculosis is a chronic disease that displays several features commonly associated with biofilm-associated infections: immune system evasion, antibiotic treatment failures, and recurrence of infection. However, although Mycobacterium tuberculosis (Mtb) can form cellulose-containing biofilms in vitro, it remains unclear whether biofilms are formed during infection in vivo. Here, we demonstrate the formation of Mtb biofilms in animal models of infection and in patients, and that biofilm formation can contribute to drug tolerance. First, we show that cellulose is also a structural component of the extracellular matrix of in vitro biofilms of fast and slow-growing nontuberculous mycobacteria. Then, we use cellulose as a biomarker to detect Mtb biofilms in the lungs of experimentally infected mice and non-human primates, as well as in lung tissue sections obtained from patients with tuberculosis. Mtb strains defective in biofilm formation are attenuated for survival in mice, suggesting that biofilms protect bacilli from the host immune system. Furthermore, the administration of nebulized cellulase enhances the antimycobacterial activity of isoniazid and rifampicin in infected mice, supporting a role for biofilms in phenotypic drug tolerance. Our findings thus indicate that Mtb biofilms are relevant to human tuberculosis.

Date: 2021
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DOI: 10.1038/s41467-021-21748-6

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