Understanding the Host Immune Response Against Mycobacterium tuberculosis Infection

149 Pages·2018·2.55 MB·English

by  Vishwanath Venketaraman

Vishwanath Venketaraman Editor
Understanding
the Host Immune
Response Against
Mycobacterium
tuberculosis Infection
Understanding the Host Immune Response Against
Mycobacterium tuberculosis Infection
Vishwanath Venketaraman
Editor
Understanding the Host
Immune Response Against
Mycobacterium tuberculosis
Infection
Editor
Vishwanath Venketaraman
Department of Basic Medical Sciences
Western University of Health Sciences
Pomona, CA, USA
ISBN 978-3-319-97366-1 ISBN 978-3-319-97367-8 (eBook)
https://doi.org/10.1007/978-3-319-97367-8
Library of Congress Control Number: 2018955426
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Preface
According to the World Health Organization, approximately a third of the world
population is latently infected with Mycobacterium tuberculosis (M. tb [LTBI]),
with an estimated 9 million individuals with active tuberculosis (TB). It is estimated
that approximately 2 million individuals die each year from active TB. In particular,
14.4% of these individuals have HIV and M. tb coinfection. Approximately 50–60%
of these individuals with HIV and M. tb coinfection are from sub-Saharan Africa.
HIV and M. tb coinfection continue to burden health-care systems in developing
countries in both African and Asian subcontinent.
M. tb infection begins when individuals inhale infectious aerosol droplets con-
taining M. tb. The inhaled bacilli are phagocytized by alveolar macrophages which
are believed to provide the first line of defense against M. tb infection. TNF released
by M. tb-infected macrophages is responsible for the formation and maintenance of
granuloma, a critical immune response required to restrict and localize M. tb infec-
tion in the lungs, thereby preventing systemic dissemination of M. tb infection to
other parts of the body.
Studies have shown that the T-helper 1 (Th1) subset of CD4+ T cell immunity
plays an important role in augmenting the effector functions of macrophages to
combating M. tb infection. It is believed that 90% of the healthy individuals mount
an effective immune response against M. tb infection in the lungs, causing the bac-
teria to become dormant inside the granuloma, and this condition is referred to as
LTBI.
M. tb is one of the leading causes of death in HIV-infected individuals. Chronic
stages of HIV infection are usually accompanied by a progressive decline in the
number of CD4+ T cells, which leads to disruption in the macrophage effector func-
tions and weakened granulomatous responses against M. tb causing active TB. In
HIV-TB coinfected individuals, M. tb can also systemically disseminate to other
parts of the body to cause extrapulmonary TB. Recent evidence indicates that indi-
viduals with type 2 diabetes are increasingly susceptible to M. tb infection. Elderly
individuals and chronic smokers are also at high risk for acquiring M. tb infection.
Understanding the effects of chronic conditions such as HIV, diabetes, chronic
cigarette smoking, and aging, in dampening the immune responses will provide
v
vi Preface
valuable information on the protective effector mechanisms that are key for defense
against M. tb infection. This textbook provides a detailed review covering recent
advances on topics such as:
1. Diabetes and TB
2. TB immunodiagnosis
3. Granulomatous responses to Mycobacterium tuberculosis infection
4. Animal models for tuberculosis
5. Host-directed therapies for tuberculosis
6. Cigarette smoking and increased susceptibility to tuberculosis
7. Coinfection with Mycobacterium tuberculosis and HIV
Pomona, CA, USA Vishwanath Venketaraman
Contents
Diabetes and Tuberculosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Blanca I. Restrepo
Recent Advances in Tuberculosis Immunodiagnostics . . . . . . . . . . . . . . . . 23
Imran H. Khan
Granulomatous Response to Mycobacterium tuberculosis Infection . . . . . 41
Afsal Kolloli, Pooja Singh, and Selvakumar Subbian
Animal Models of Tuberculosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
Pooja Singh, Afsal Kolloli, and Selvakumar Subbian
Novel Antimycobacterial Drugs and Host- Directed Therapies
for Tuberculosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99
Garrett Teskey, Caleb Cato, Jennifer Hernandez, Preet Kaur, Jeff Koury,
Mariana Lucero, Andrew Tran, and Vishwanath Venketaraman
Cigarette Smoking and Increased Susceptibility to Mycobacterium
tuberculosis Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
John Brazil and Vishwanath Venketaraman
Coinfection with Mycobacterium tuberculosis and HIV . . . . . . . . . . . . . . . 127
Luke Elizabeth Hanna
vii
Contributors
John Brazil The Master’s University, Santa Clarita, CA, USA
Caleb Cato Graduate College of Biomedical Sciences, Western University of
Health Sciences, Pomona, CA, USA
Luke Elizabeth Hanna National Institute for Research in Tuberculosis, Chennai,
India
Jennifer Hernandez Graduate College of Biomedical Sciences, Western University
of Health Sciences, Pomona, CA, USA
Preet Kaur Graduate College of Biomedical Sciences, Western University of
Health Sciences, Pomona, CA, USA
Imran H. Khan Department of Pathology and Laboratory Medicine, School of
Medicine, University of California Davis Health System, Sacramento, CA, USA
Afsal Kolloli Public Health Research Institute, New Jersey Medical School at
Rutgers Biomedical and Health Sciences, Rutgers University, Newark, NJ, USA
Jeff Koury Graduate College of Biomedical Sciences, Western University of
Health Sciences, Pomona, CA, USA
Mariana Lucero Graduate College of Biomedical Sciences, Western University of
Health Sciences, Pomona, CA, USA
Blanca I. Restrepo UTHealth Houston, School of Public Health, Brownsville, TX,
USA
Pooja Singh Public Health Research Institute, New Jersey Medical School at
Rutgers Biomedical and Health Sciences, Rutgers University, Newark, NJ, USA
Selvakumar  Subbian Public Health Research Institute, New Jersey Medical
School at Rutgers Biomedical and Health Sciences, Rutgers University, Newark,
NJ, USA
ix
x Contributors
Garrett Teskey Graduate College of Biomedical Sciences, Western University of
Health Sciences, Pomona, CA, USA
Andrew Tran Graduate College of Biomedical Sciences, Western University of
Health Sciences, Pomona, CA, USA
Vishwanath Venketaraman Graduate College of Biomedical Sciences, Western
University of Health Sciences, Pomona, CA, USA
Department of Basic Medical Sciences, College of Osteopathic Medicine of the
Pacific, Western University of Health Sciences, Pomona, CA, USA
Diabetes and Tuberculosis
Blanca I. Restrepo
Diabetes mellitus is characterized by hyperglycemia due to defects in insulin secre-
tion, insulin response, or both (American-Diabetes-Association 2014). Type 1 and
type 2 diabetes (T2D) patients have a higher morbidity and mortality from pulmo-
nary infections, with tuberculosis (TB) being a prominent example (Muller et al.
2005; Shah and Hux 2003). In this chapter the focus is mostly on T2D which is the
most prevalent form. The worldwide increase in the prevalence of T2D in low- and
middle-income countries where TB is most endemic is a recognized reemerging risk
and challenge to TB control (Ottmani et al. 2010). Individuals with T2D have three
times the risk of developing TB, and there are now more individuals with TB-T2D
comorbidity than TB-HIV coinfection (Jeon and Murray 2008; Ronacher et al.
2015). The frequent co-occurrence of diabetes (type 1 or type 2) and TB was first
described centuries ago by the Persian philosopher Avincenna. The comorbidity was
a frequent topic in the medical literature in the first half of the twentieth century, but
its notoriety was reduced with the introduction of insulin treatment for type 1 diabe-
tes and antibiotics for TB (Boucot et al. 1952; Morton 1694; Root 1934; Silwer and
Oscarsson 1958). In the 1980s, the publications on joint TB-T2D began to reappear
with the number of publications on TB and T2D rising exponentially in contempo-
rary times as the global prevalence of T2D among adults has continued to rise
(Fig. 1). Diabetes is predicted to reach 642 million worldwide by 2040 with most
(80%) of the patients living in low- and middle-income countries where TB is also
endemic (International-Diabetes-Federation 2015). The World Health Organization
has identified T2D as a neglected, important, and reemerging risk factor for TB
(Ottmani et al. 2010). In this chapter, “T2D” will refer mostly to type 2 diabetes since
it is the most prevalent form, but type 1 diabetes in children has also been associated
with TB (International-Diabetes-Federation 2015; Webb et al. 2009). This chapter
B. I. Restrepo (*)
UTHealth Houston, School of Public Health, Brownsville, TX, USA
e-mail: [e-mail]
© Springer Nature Switzerland AG 2018 1
V. Venketaraman (ed.), Understanding the Host Immune Response Against
Mycobacterium tuberculosis Infection, https://doi.org/10.1007/978-3-319-97367-8_1