Author Correction: Reprogramming of host glutamine metabolism during Chlamydia trachomatis infection and its key role in peptidoglycan synthesis

Rajeeve, Karthika; Vollmuth, Nadine; Janaki‐Raman, Sudha; Wulff, Thomas F.; Baluapuri, Apoorva; Dejure, Francesca R.; Huber, Claudia; Fink, J. Stephen; Schmalhofer, Maximilian; Schmitz, W.; Sivadasan, Rajeeve; Eilers, Martin; Wolf, Elmar; Eisenreich, Wolfgang; Schulze, Almut; Seibel, Jürgen; Rudel, Thomas

doi:10.1038/s41564-021-00874-3

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“…Moreover, C. trachomatis also downregulates the tumour suppressor p53 [27,31] via the PI3K and MDM2 pathways. The bacteria induce glutamine addiction in the infected cells by stabilizing the proto-oncogene c-Myc [26]. In addition, the infection remains asymptomatic by paralyzing the neutrophils, the first line of defense [32].…”

Section: Chlamydia Trachomatis and Pneumoniaementioning

confidence: 99%

Bacteria–Cancer Interface: Awaiting the Perfect Storm

Hansen¹,

Ali²,

Sivadasan

et al. 2021

Pathogens

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Epidemiological evidence reveal a very close association of malignancies with chronic inflammation as a result of persistent bacterial infection. Recently, more studies have provided experimental evidence for an etiological role of bacterial factors disposing infected tissue towards carcinoma. When healthy cells accumulate genomic insults resulting in DNA damage, they may sustain proliferative signalling, resist apoptotic signals, evade growth suppressors, enable replicative immortality, and induce angiogenesis, thus boosting active invasion and metastasis. Moreover, these cells must be able to deregulate cellular energetics and have the ability to evade immune destruction. How bacterial infection leads to mutations and enriches a tumour-promoting inflammatory response or micro-environment is still not clear. In this review we showcase well-studied bacteria and their virulence factors that are tightly associated with carcinoma and the various mechanisms and pathways that could have carcinogenic properties.

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