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Hajjar, S., & Zhou, X. (2023). Ph sensing at the intersection of tissue homeostasis and inflammation. Trends in Immunology, 44(10), 807–825. 
Added by: Dr. Enrique Feoli (03/07/2025, 21:37)   Last edited by: Dr. Enrique Feoli (21/04/2026, 14:27)
Resource type: Journal Article
DOI: 10.1016/j.it.2023.08.008
ID no. (ISBN etc.): 1471-4906
BibTeX citation key: Hajjar2023
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 Categories: BioAcyl Corp, BioAcyl Corp
Subcategories: Extracellular acidity, Microenvironment
Keywords: acidic environment, adaptation, inflammatory response, pH homeostasis, pH sensing, resistance
Creators: Hajjar, Zhou
Collection: Trends in Immunology		 Views: 7/34
Abstract
pH is tightly maintained at cellular, tissue, and systemic levels, and altered pH – particularly in the acidic range – is associated with infection, injury, solid tumors, and physiological and pathological inflammation. However, how pH is sensed and regulated and how it influences immune responses remain poorly understood at the tissue level. Applying conceptual frameworks of homeostatic and inflammatory circuitries, we categorize cellular and tissue components engaged in pH regulation, drawing parallels from established cases in physiology. By expressing various intracellular (pHi) and extracellular pH (pHe)-sensing receptors, the immune system may integrate information on tissue and cellular states into the regulation of homeostatic and inflammatory programs. We introduce the novel concept of resistance and adaptation responses to rationalize pH-dependent immunomodulation intertwined with homeostatic equilibrium and inflammatory control. We discuss emerging challenges and opportunities in understanding the immunological roles of pH sensing, which might reveal new strategies to combat inflammation and restore tissue homeostasis.
  
Notes

 

The homeostatic circuit comprises four major components: regulated variables, sensors, homeostatic 
signals, and effectors. Deviations in regulated variables (such as pH or oxygen) from a set-point can 
be monitored by homeostatic sensors and corrected by effectors through a feedback mechanism. In 
parallel, the inflammatory circuit is initiated by sensing an inflammatory trigger (such as molecular 
cues of an infection or injury) by the sensor cells (e.g., macrophages, dendritic cells, airway epithelial 
cells). Inflammatory signals produced from the sensor cells can act on various cell types within a 
target tissue, activating inflammatory cascades and modulating tissue physiology to eliminate the 
inflammatory triggers as negative feedback. As a consequence of inflammation, many environmental 
variables, including pH, oxygen, lactate are perturbed from homeostatic range. Sensing the deviation 
of critical tissue microenvironment variables can serve as tunable feedback to limit tissue damage.


Added by: Dr. Enrique Feoli  Last edited by: Dr. Enrique Feoli
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