Lipid larceny: channelizing host lipids for establishing successful pathogenesis by bacteria

Abstract

Lipids are complex organic compounds made up of carbon, oxygen, and hydrogen. These play a diverse and intricate role in cellular processes like membrane trafficking, protein sorting, signal transduction, and bacterial infections. Both Gram-positive bacteria (Staphylococcus sp., Listeria monocytogenes, etc.) and Gram-negative bacteria (Chlamydia sp., Salmonella sp., E. coli, etc.) can hijack the various host-lipids and utilize them structurally as well as functionally to mount a successful infection. The pathogens can deploy with various arsenals to exploit host membrane lipids and lipid-associated receptors as an attachment for toxins' landing or facilitate their entry into the host cellular niche. Bacterial species like Mycobacterium sp. can also modulate the host lipid metabolism to fetch its carbon source from the host. The sequential conversion of host membrane lipids into arachidonic acid and prostaglandin E2 due to increased activity of cPLA-2 and COX-2 upon bacterial infection creates immunosuppressive conditions and facilitates the intracellular growth and proliferation of bacteria. However, lipids' more debatable role is that they can also be a blessing in disguise. Certain host-lipids, especially sphingolipids, have been shown to play a crucial antibacterial role and help the host in combating the infections. This review shed light on the detailed role of host lipids in bacterial infections and the current understanding of the lipid in therapeutics. We have also discussed potential prospects and the need of the hour to help us cope in this race against deadly pathogens and their rapidly evolving stealthy virulence strategies.

Helicobacter pylori cholesterol-α-glucosyltransferase manipulates cholesterol for bacterial adherence to gastric epithelial cells

“…Lipid rafts are membrane cholesterol-rich microdomains that provide entry portals for many bacterial pathogens or their virulence factors [15]. Both CagA translocation and VacA delivery into host cells following H. pylori infection require lipid rafts [16][17][18].…”

Giardial lipid rafts share virulence factors with secreted vesicles and participate in parasitic infection in mice

“…Studies also indicate that MBCD, a cholesterol-binding agent and a common LR inhibitor, blocks the attachment of trophozoites on cultured Caco-2 cells ( Humen et al., 2011 ), implicating that giardial attachment to host cells is likely to be linked to gLRs. Attachment through LRs has also been reported in case of human sperm cells on oocytes ( Van Blerkom and Caltrider, 2013 ), and evidence suggests that LRs regulate bacterial attachment and viral entry into host cells ( Chatterjee et al., 2021 ; Palacios-Rápalo et al., 2021 ). It been demonstrated that, MBCD blocks microvesicles biogenesis as well as attachment to CaCo-2 cells by Giardia ( Evans-Osses et al., 2017 ), further supporting the idea that LRs, giardial attachment, and vesicle biogenesis are interdependent.…”

Molecular Mechanisms of Lipid Metabolism Disorders in Infectious Exacerbations of Chronic Obstructive Pulmonary Disease

“…A growing body of evidence leaves no doubt that some bacteria and viruses use the lipid microdomains of the plasma membrane for interaction, binding, and possible penetration into cells [ 164 , 165 ]. Some pathogens can affect the lipid metabolism in the host cells by realizing their virulence, as well as using the host lipids as a food source or assimilating them into their metabolic or structural processes [ 280 ]. For colonization of the lungs in COPD bacteria use many other strategies, including modification of the lipid composition of the membrane, which affects its permeability for antibacterial drugs, the formation of biofilms, and the exclusion of certain lipids from the host metabolic and immune processes [ 281 ].…”