Heat Shock Proteins (HSPs): The Silent Protectors of Chicken Cells

Heat stress is a widespread and serious issue that affects not only the behaviour of chickens but every single cell in their bodies. From the outside, this may appear as reduced feed intake, smaller egg size, or lower shell quality. However, these visible effects are the outward signs of a silent defence mechanism working at the cellular level.

One of the most critical elements of this defence system is the group of heat shock proteins (HSPs), which are molecules that often go unnoticed but play vital protective roles.

What Are Heat Shock Proteins (HSPs)?

Heat shock proteins (HSPs) are specialised protective proteins produced by cells under stress conditions such as high temperature. First discovered in fruit flies in the 1960s, they have since been identified in almost all living organisms performing similar protective functions.

Within the cell, HSPs act as a kind of “maintenance and repair team.” Under normal conditions, they are present at low levels; but when a cell detects danger, their production rapidly increases to perform the following tasks:

• Repair or refold damaged proteins.
• Eliminate misfolded or toxic proteins.
• Ensure proper folding of newly synthesised proteins.
• Help maintain cellular balance (homeostasis).

Activation of HSPs During Heat Stress

Unlike mammals, chickens cannot regulate their body temperature by sweating. Their physiological responses are limited to panting and other minor adjustments. Therefore, cellular defence mechanisms play a crucial role in their survival.

The heat stress response at the cellular level functions as follows:

1. Rising temperature disrupts the structural integrity of intracellular proteins (denaturation).
2. This triggers stress signals and activates HSP genes.
3. HSP production increases, and these proteins restructure damaged ones or neutralise their toxic effects.
4. As a result, the cell restores temporary balance and maintains functionality.

Particularly HSP70 and HSP90 are synthesised intensively in metabolically and immunologically active tissues such as the liver, intestines, brain, and immune organs. This enables cells to resist short-term heat stress and survive without damage.

Functions of HSP70 and HSP90

Among all heat shock proteins, HSP70 and HSP90 are the best studied and most crucial. They act as molecular chaperones: proteins that ensure correct folding, repair damaged structures, and maintain intracellular balance.

HSP70: The First Response Team

HSP70 is the fastest and strongest component of the cellular response to heat stress. Its synthesis can increase within minutes of stress detection.

Main functions of HSP70:

• Refolds and restores the function of damaged proteins.
• Assists the proper folding of newly synthesised proteins.
• Recognises and marks defective or toxic proteins for degradation.
• Works intensively in intestinal epithelial cells, reducing heat-induced intestinal permeability.

If heat stress persists and HSP70 synthesis becomes insufficient, protein accumulation begins, potentially triggering cell death.

HSP90: The System Regulator

HSP90 primarily regulates intracellular communication and signalling pathways, playing roles in many biological processes:

• Stabilises critical proteins such as steroid receptors, growth factors, and kinases.
• Controls cell cycle progression and division.
• Keeps inflammatory signalling under control, maintaining a balanced immune response.

HSP90 is particularly important in metabolically active organs such as the liver, lymphoid tissues, and brain.

Chronic Stress and HSP Imbalance

While HSPs are highly effective against acute stress, their protective capacity has limits. Under chronic heat stress, their production and function can be severely disrupted.

Main cellular effects include:

• Increased energy demand: Continuous HSP production consumes large amounts of energy, reducing resources for other cellular functions.
• Oxidative stress: Reduced mitochondrial protection leads to the accumulation of reactive oxygen species (ROS) and oxidative damage.
• Protein imbalance: Accumulated damaged proteins impair cellular processes and increase toxicity.
• Immune suppression: Overactivation of the HSP system weakens immune cell functions and increases susceptibility to infections.

Observed physiological effects in chickens:

• Egg quality deterioration: Thinner shells, higher breakage rates, and reduced egg weight.
• Reduced feed efficiency: Impaired intestinal barrier function and nutrient absorption.
• Immunosuppression: Lymphoid tissue atrophy, reduced antibody response, increased disease susceptibility.
• Overall performance decline: Energy diverted from growth and reproduction to stress management.

The HPA Axis and Its Relationship with HSPs

Heat stress triggers both systemic and cellular responses in chickens. These two are closely linked: while the HPA axis (hypothalamic–pituitary–adrenal) governs hormonal stress responses, HSPs act as cellular defenders.

Activation of the HPA axis releases corticosterone and other stress hormones. These regulate metabolism but can also stimulate HSP gene expression, showing that cellular stress signals are triggered not only by temperature but also through hormonal pathways.

This interaction enables a multilayered defence mechanism:

• The HPA axis prepares the whole organism.
• HSPs minimise damage at the cellular level.

However, prolonged activation exhausts both systems, leading to weakened immunity, lower performance, and loss of cellular integrity.

Silent but Critical Resistance

In laying hens, heat stress becomes a complex physiological crisis rather than a simple reaction to rising temperature. The HPA axis and HSPs work together to maintain stability: while one manages systemic responses, the other safeguards cells. HSP70 and HSP90 prevent protein damage, preserve cellular structure, and protect against cell death.

Yet the success of this system depends on the intensity and duration of stress. When exposure is chronic, HSP defences falter, leading to immune suppression, oxidative stress, reduced performance, and reproductive issues. Therefore, strategies to combat heat stress must address not only external conditions but also cellular resilience.

Effective Management Strategies Against Heat Stress

• Feed during cooler hours of the day.
• Ensure efficient operation of climate control systems.
• Provide constant access to clean, cool drinking water; add electrolytes or vitamin C when needed.
• Use antioxidant supplements to reduce oxidative load.
• Support gut integrity with appropriate additives.
• Reduce stocking density during high-temperature periods.
• Adjust lighting programmes to minimise stress behaviours.