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Prolonged Humid Heat Triggers Systemic Inflammation and Stress Signaling: Fluid Intake Modulates NF-κB, p38, JNK2,

Faming Wang1, Caiping Lu1, Ying Lei1

  • 1Centre for Molecular Biosciences and Non-Communicable Diseases, School of Safety Science and Engineering, Xi'an University of Science and Technology (XUST), Xi'an 710054, China.

International Journal of Molecular Sciences
|June 13, 2025
PubMed
Summary

Adequate hydration significantly reduces core body temperature and mitigates inflammation, organ stress, and hormonal imbalance during prolonged humid heat exposure. Full fluid intake (FFI) suppressed key molecular stress pathways, unlike limited fluid intake (LFI).

Keywords:
fluid intakeinflammatory signaling pathwayrenal and hepatic stresssystemic inflammation

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Area of Science:

  • Environmental Physiology
  • Human Physiology
  • Climate Health

Background:

  • Extreme humid heat exposure poses significant health risks, including systemic inflammation, organ stress, and hormonal imbalance.
  • While fluid replacement is a common strategy, its precise impact on physiological responses during humid heat stress requires further elucidation.
  • Understanding hydration's role is crucial for developing effective preventive measures against heat-related illnesses.

Purpose of the Study:

  • To investigate the effects of limited fluid intake (LFI) versus full fluid intake (FFI) on thermoregulation, inflammation, organ function, and stress signaling during prolonged humid heat exposure.
  • To determine the mechanistic efficacy of hydration in attenuating physiological and molecular stress responses to heat.

Main Methods:

  • A randomized controlled trial involving 32 healthy adults exposed to 8 hours of humid heat (40 °C, 55% RH) under LFI (125 mL/h) and FFI (375 mL/h) conditions.
  • Assessment of core body temperature, inflammatory cytokines (IL-6, IL-1β, IFN-γ, TNF-α), organ stress markers (ALT, BUN), oxidative stress indices (MDA, SOD), and cortisol.
  • Analysis of molecular signaling pathways (NF-κB, JNK, p38, STAT3) in peripheral blood mononuclear cells (PBMCs) via Western blot.

Main Results:

  • Full fluid intake (FFI) significantly reduced post-exposure core body temperature compared to limited fluid intake (LFI).
  • FFI effectively mitigated elevations in inflammatory cytokines, blood urea nitrogen (BUN), alanine aminotransferase (ALT), and cortisol levels.
  • LFI activated key stress-related signaling pathways (NF-κB, JNK, p38, STAT3 phosphorylation) in PBMCs, whereas FFI suppressed these responses.

Conclusions:

  • Adequate hydration is a critical factor in attenuating systemic and molecular stress responses induced by prolonged humid heat exposure.
  • Hydration modulates inflammatory signaling pathways, highlighting its importance in preventing heat-related physiological strain.
  • These findings underscore the significance of maintaining sufficient fluid intake for populations exposed to extreme heat events, particularly in the context of climate change.