Bacterial stress response: understanding the molecular mechanics to identify possible therapeutic targets

ABSTRACT

Introduction

Bacteria are ubiquitous and many of them are pathogenic in nature. Entry of bacteria in host and its recognition by host defense system induce stress in host cells. With time, bacteria have also developed strategies including drug resistance to escape from antibacterial therapy as well as host defense mechanism.

Areas covered

Bacterial stress initiates and promotes adaptive immune response through several integrated mechanisms. The mechanisms of bacteria to up and down regulate different pathways involved in these responses have been discussed. The genetic expression of these pathways can be manipulated by the pharmacological interventions. Present review discusses in these contexts and explores the possibilities to overcome stress induced by bacterial pathogens and to suggest new possible therapeutic targets.

Expert opinion

In our opinion, there are two important fronts to regulate the bacterial stress. One is to target caspase involved in the process of transformation and translation at gene level and protein expression. Second is the identification of bacterial genes that lead to synthesis of abnormal end products supporting bacterial survival in host environment and also to surpass the host defense mechanism. Identification of such genes and their expression products could be an effective option to encounter bacterial resistance.

KEYWORDS:

• Bacterial stress
• PAMPs
• PRRs
• eIF-2α
• ATF4
• integrated stress response
• xenophagy
• therapeutic efficacy

Article highlights

• Entry and survival of bacteria in host induce stress to the host system.

• Bacteria develop strategies to surpass host defense system.

• Resistance against antibacterial has imposed serious public health threat.

• Caspase involved in transformation and translation are potential therapeutic targets.

• Manipulation of expression of drug resistance genes can also be an effective option.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.