Inflammatory response is an important driving factor in the occurrence and development of mastitis. The production and release of cytokines plays a leading role in the process of inflammatory response. Both acute and chronic inflammatory reactions will cause the release of cytokines, and the excessive release of cytokines will aggravate the inflammatory process and accelerate the disease process. During the occurrence and development of mastitis, the production and release of cytokines, the integrity of blood milk barrier and the disease process of mastitis are closely related.
Mastitis is mainly caused by various endogenous or exogenous factors, such as bacterial invasion, tumor, mechanical stress and so on. Various endogenous or exogenous factors can activate damage-associated molecular pattern (DAMPs) on cell membrane surface, such as toll like receptors, or directly activate inflammasomes such as NLRP3, AIM2 and NLRP1, resulting in the release of inflammatory cytokines. Inflammatory cytokines recruit immune cells from all over the body to enter the mammary gland, and the immune cells gathered in the mammary gland will continue to release a large amount of inflammatory cytokines after receiving stimulation. The immune cells over activated by inflammatory cytokines may mediate cell death, apoptosis or necrosis through caspase-3, caspase-1 and other pathways. Dead immune cells will lead to the uncontrolled release of cytokines into the mammary microenvironment, which will mediate mammary injury, and even cause cytokine storm, which is life-threatening.
The pro-inflammatory cytokines released by immune cells will not only affect the immune cells themselves, but also further destroy the blood milk barrier in the mammary gland. Mammary epithelial cells are important cell groups that maintain the normal physiological function of mammary gland and form the blood milk barrier. In the process of mastitis, the excessive release of cytokines will seriously destroy mammary epithelial cells. IL-6, IL-1ß and other pro-inflammatory cytokines can activate the receptors of mammary epithelial cells, such as IL-1RI, and then activate the NF-?B, JNK and p38 signal pathway, resulting in inflammatory damage of mammary epithelial cells.
Although the results of cytokine destruction of mammary gland have been reported, how cytokines are formed and released in immune cells or epithelial cells, and the specific mechanism of cytokine destruction of blood milk barrier need to be deeply explored. Therefore, our theme is to reveal the formation mechanism of cytokines in cells, the release mechanism of cytokines and the destruction mechanism of cytokines on blood milk barrier.
We welcome submissions of Original Research, Review and Mini Review on the sub-topics below:
1) Formation mechanism of intracellular cytokines,
2) Release mechanism of cytokines,
3) Mechanism of cytokines on destroying blood milk barrier,
4) Mechanism of action in relieving mastitis and screening of small molecule compounds.
Inflammatory response is an important driving factor in the occurrence and development of mastitis. The production and release of cytokines plays a leading role in the process of inflammatory response. Both acute and chronic inflammatory reactions will cause the release of cytokines, and the excessive release of cytokines will aggravate the inflammatory process and accelerate the disease process. During the occurrence and development of mastitis, the production and release of cytokines, the integrity of blood milk barrier and the disease process of mastitis are closely related.
Mastitis is mainly caused by various endogenous or exogenous factors, such as bacterial invasion, tumor, mechanical stress and so on. Various endogenous or exogenous factors can activate damage-associated molecular pattern (DAMPs) on cell membrane surface, such as toll like receptors, or directly activate inflammasomes such as NLRP3, AIM2 and NLRP1, resulting in the release of inflammatory cytokines. Inflammatory cytokines recruit immune cells from all over the body to enter the mammary gland, and the immune cells gathered in the mammary gland will continue to release a large amount of inflammatory cytokines after receiving stimulation. The immune cells over activated by inflammatory cytokines may mediate cell death, apoptosis or necrosis through caspase-3, caspase-1 and other pathways. Dead immune cells will lead to the uncontrolled release of cytokines into the mammary microenvironment, which will mediate mammary injury, and even cause cytokine storm, which is life-threatening.
The pro-inflammatory cytokines released by immune cells will not only affect the immune cells themselves, but also further destroy the blood milk barrier in the mammary gland. Mammary epithelial cells are important cell groups that maintain the normal physiological function of mammary gland and form the blood milk barrier. In the process of mastitis, the excessive release of cytokines will seriously destroy mammary epithelial cells. IL-6, IL-1ß and other pro-inflammatory cytokines can activate the receptors of mammary epithelial cells, such as IL-1RI, and then activate the NF-?B, JNK and p38 signal pathway, resulting in inflammatory damage of mammary epithelial cells.
Although the results of cytokine destruction of mammary gland have been reported, how cytokines are formed and released in immune cells or epithelial cells, and the specific mechanism of cytokine destruction of blood milk barrier need to be deeply explored. Therefore, our theme is to reveal the formation mechanism of cytokines in cells, the release mechanism of cytokines and the destruction mechanism of cytokines on blood milk barrier.
We welcome submissions of Original Research, Review and Mini Review on the sub-topics below:
1) Formation mechanism of intracellular cytokines,
2) Release mechanism of cytokines,
3) Mechanism of cytokines on destroying blood milk barrier,
4) Mechanism of action in relieving mastitis and screening of small molecule compounds.