Inflammatory Response I: Vascular and Cellular

The inflammatory response is a defense mechanism against infection, injury, or irritation from bacteria, trauma, toxins, or heat. It helps locate and destroy pathogens while removing damaged tissue elements to promote healing. This response occurs at both vascular and cellular levels, with fluid, blood products, and nutrients migrating to the injured area, resulting in redness, heat, swelling, pain, and loss of function.

During the vascular stage, small blood vessels near the injury site initially constrict to prevent blood loss. The arterioles and venules then dilate, increasing blood flow and causing local redness and heat. Cell mediators like histamine and bradykinin are released, increasing vascular permeability and allowing protein-rich fluids to flow into the area, causing swelling and pain.

During the cellular stage, white blood cells, including neutrophils and monocytes, pass through blood vessels and rush to the injury site, increasing overall WBC count. These cells engulf pathogens through phagocytosis and ingest cell debris and foreign material. This phagocytic activity releases pyrogens from bacterial cells, which trigger fever as part of the systemic inflammatory response.

Cell mediators such as histamine, bradykinin, and prostaglandins are released in the injured area during inflammation. These mediators increase vascular permeability, allowing protein- and immune-cell-rich fluids to escape blood vessels and enter surrounding tissue. This fluid accumulation causes the characteristic swelling, pain, and temporary loss of function associated with acute inflammation.

Inflammation can be acute, lasting days or weeks, or chronic, lasting several months to years. Acute inflammation is the initial response to injury or infection, characterized by vascular and cellular changes. Chronic inflammation represents a prolonged response when the body cannot fully resolve the initial insult, potentially leading to tissue damage and systemic complications.

Systemic inflammation produces signs beyond the local injury site, including fever, increased white blood cell count, malaise, anorexia, nausea, and vomiting. Lymph node enlargement may also occur as lymphoid tissues respond to infection. In severe cases, organ failure can develop, indicating that the inflammatory response has become widespread and potentially harmful.

Fever develops when white blood cells engulf pathogens through phagocytosis during the cellular stage of inflammation. This phagocytic activity releases pyrogens from bacterial cells, which are fever-inducing substances. Pyrogens circulate through the bloodstream and act on the body's temperature-regulating center, raising the set point and causing fever as part of the systemic inflammatory defense.