Nutritional status positively impacts humoral immunity against its Mycobacterium tuberculosis, disease progression, and vaccine development

PLoS One. 2020 Aug 6;15(8):e0237062. doi: 10.1371/journal.pone.0237062. eCollection 2020.

Abstract

Nutritional status contributes to the regulation of immune responses against pathogens, and malnutrition has been considered as a risk factor for tuberculosis (TB). Mycobacterium tuberculosis (Mtb), the causative agent of TB, can modulate host lipid metabolism and induce lipid accumulation in macrophages, where the bacilli adopt a dormant phenotype. In addition, serum lipid components play dual roles in the regulation of and protection from Mtb infection. We analyzed the relationship between nutritional status and the humoral immune response in TB patients. We found that serum HDL levels are positively correlated with the serum IgA specific for Mtb antigens. Analysis of the relationship between serum nutritional parameters and clinical parameters in TB patients showed that serum albumin and CRP levels were negatively correlated before treatment. We also observed reduced serum LDL levels in TB patients following treatment. These findings may provide insight into the role of serum lipids in host immune responses against Mtb infection. Furthermore, improving the nutritional status may enhance vaccination efficacy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Antibodies, Bacterial / blood
  • C-Reactive Protein / metabolism
  • Disease Progression
  • Female
  • Humans
  • Immunity, Humoral*
  • Lipids / blood
  • Male
  • Middle Aged
  • Mycobacterium tuberculosis / immunology*
  • Nutritional Status / immunology*
  • Serum Albumin, Human / metabolism
  • Tuberculosis Vaccines / immunology
  • Tuberculosis, Pulmonary / blood
  • Tuberculosis, Pulmonary / drug therapy
  • Tuberculosis, Pulmonary / immunology*

Substances

  • Antibodies, Bacterial
  • Lipids
  • Tuberculosis Vaccines
  • C-Reactive Protein
  • Serum Albumin, Human

Grants and funding

The authors are thankful to all healthcare workers and tuberculosis patients who participated in this study. This work was supported in part by AMED under Grant Number JP18FK0108075 (to Y. H.) and by a Grant-in- Aid for Scientific Research (C) from the Japan Society for the Promotion of Science for Mam. N. (16K09584) and Y. H. (18K08312). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.