Inflammation is your immune system’s response to something it perceives as harmful, whether that’s a bacterial infection, a splinter, a poor diet, or your own stressed-out biology. It starts as a protective mechanism: immune cells rush to the site of trouble, blood vessels widen to let them through, and signaling molecules coordinate the cleanup. Problems arise when this response fires too often, too intensely, or never fully shuts off. The causes range from obvious infections and injuries to subtler triggers like excess body fat, chronic stress, and the food you eat every day.
Infections and Physical Injury
The most straightforward cause of inflammation is infection. Your immune cells carry surface receptors that recognize structural signatures unique to bacteria, viruses, and fungi. Gram-negative bacteria, for instance, have a molecule called lipopolysaccharide in their outer walls that your immune system detects almost immediately. Viruses trigger the same alarm system through their genetic material. Once these foreign signatures are detected, your cells launch a cascade of signaling molecules that recruit more immune cells, raise local temperature, and increase blood flow to the area.
Physical injury works through a parallel pathway. When cells are crushed, torn, or starved of oxygen, they spill their internal contents into surrounding tissue. These leaked molecules, including fragments of DNA, proteins, and metabolic byproducts, act as distress signals. Your immune system treats them much like it treats an invading pathogen: it sends in first responders to clear debris and begin repairs. This is why a sprained ankle swells and a surgical incision turns red and warm. The inflammation is doing exactly what it should.
How the Inflammatory Cascade Works
Once your immune system detects a threat, it communicates through small signaling proteins called cytokines. Two of the most important are TNF-alpha and IL-6. TNF-alpha is one of the first to arrive at the scene. It triggers nearby cells to produce adhesion molecules on blood vessel walls, essentially creating sticky patches that help immune cells grab hold and migrate into damaged tissue. TNF-alpha also stimulates the production of IL-6, which activates a broader immune response by switching on both T and B cells, two key players in adaptive immunity.
This cascade is tightly regulated in a healthy system. Once the threat is neutralized, anti-inflammatory signals ramp up and the process winds down within hours to a few days. Acute inflammation, the kind you get from a cut or a cold, typically resolves in that timeframe. Chronic inflammation, by contrast, persists for months or years, often at a low, simmering level that doesn’t produce obvious swelling or redness but still damages tissue over time.
Diet and Inflammatory Foods
What you eat can directly raise or lower the level of inflammatory activity in your body. The strongest dietary drivers of inflammation include foods high in saturated fat, trans fat, added sugar, refined carbohydrates, and processed or red meat.
Trans fats are particularly harmful. They raise LDL (“bad”) cholesterol while lowering HDL (“good”) cholesterol, and research has found no safe level of consumption. Refined carbohydrates like white bread and sugary cereals spike blood sugar rapidly because they lack fiber, fat, or protein to slow digestion. That rapid spike triggers an insulin surge, which promotes a pro-inflammatory state. The same mechanism applies to diets high in simple sugars.
The balance between omega-3 and omega-6 fatty acids also matters. Omega-6s, found in many vegetable oils and processed foods, promote inflammation when they vastly outnumber omega-3s in your diet. Most Western diets are heavily skewed toward omega-6s, which helps explain why dietary changes can meaningfully reduce inflammatory markers in blood tests.
Excess Body Fat
Carrying excess weight, especially around the abdomen, is one of the most potent drivers of chronic, low-grade inflammation. Fat tissue isn’t just a passive energy reserve. It’s an active endocrine organ that releases hormones and signaling molecules directly into your bloodstream.
As fat cells expand during weight gain, they begin to die off at higher rates. Your immune system responds by sending macrophages to clean up the dead cells. These macrophages cluster around dying fat cells and, over time, shift from a neutral or anti-inflammatory state to a pro-inflammatory one. Once activated, they pump out TNF-alpha and IL-6, the same cytokines involved in infection-fighting. Fat tissue also produces resistin, a molecule originally identified as a fat-cell hormone but now understood to come largely from immune cells embedded within fat. Resistin amplifies inflammatory signaling by triggering even more TNF-alpha and IL-6 production.
This creates a self-reinforcing cycle: more fat leads to more immune cell infiltration, which leads to more inflammatory signaling, which contributes to insulin resistance, metabolic dysfunction, and increased risk of heart disease and type 2 diabetes.
Chronic Stress
Short bursts of stress temporarily suppress inflammation through cortisol, a hormone released by your adrenal glands. Cortisol acts as a natural brake on immune activity. But when stress becomes chronic, the system breaks down in a counterintuitive way: instead of keeping inflammation in check, prolonged cortisol exposure actually makes your immune cells less responsive to cortisol’s calming signal.
This phenomenon, called glucocorticoid resistance, means your body keeps pumping out cortisol, but immune cells increasingly ignore it. The normal daily rhythm of cortisol, which should peak in the morning and taper at night, becomes flattened or erratic. Brain structures involved in regulating the stress response, particularly the hippocampus and prefrontal cortex, lose sensitivity to cortisol over time, further disrupting the feedback loop that would normally shut the response down. The net result is a shift toward higher levels of inflammatory cytokines like IL-6 and TNF-alpha, with a simultaneous drop in anti-inflammatory signals. This pro-inflammatory tilt has been directly linked to increased risk of autoimmune conditions.
Air Pollution and Environmental Toxins
Breathing polluted air causes inflammation through the respiratory tract, but the effects don’t stay in your lungs. Fine particulate matter, particles small enough to measure in millionths of a meter, can penetrate deep into lung tissue, cross into the bloodstream, and travel to organs throughout the body. The World Health Organization identifies particulate matter, carbon monoxide, ozone, nitrogen dioxide, and sulfur dioxide as the pollutants with the strongest evidence of harm to human health.
These pollutants trigger oxidative stress, a state where reactive molecules overwhelm your cells’ natural defenses and damage DNA, proteins, and cell membranes. The immune system treats this damage the same way it treats an infection: it mounts an inflammatory response. Over years of exposure, this contributes to chronic inflammation affecting the lungs, heart, and brain.
Autoimmune Triggers
In autoimmune diseases, the inflammatory response turns against the body’s own tissues. Conditions like rheumatoid arthritis, lupus, and inflammatory bowel disease all involve immune cells that mistakenly attack healthy cells as though they were foreign invaders.
Research from Harvard Medical School has identified a protein called granzyme K as a key driver of this process. Granzyme K is produced by a specific group of immune cells found in high concentrations in inflamed tissues of people with autoimmune conditions. It works by activating the complement system, a network of proteins normally reserved for destroying pathogens, and redirecting it against the body’s own tissues. This generates molecules that recruit even more immune cells and cause further tissue damage, creating a cycle of escalating inflammation.
The initial triggers for autoimmunity remain complex and vary by disease, but the downstream mechanism is increasingly clear: specific immune cells produce proteins that hijack the body’s own defense systems and turn them inward.
Measuring Inflammation
If you suspect chronic inflammation, the most common screening tool is a C-reactive protein (CRP) test, a simple blood draw. CRP is a protein your liver produces in response to inflammation anywhere in the body. A normal level falls below 0.9 mg/dL. Results between 1.0 and 10.0 mg/dL indicate moderate elevation, which can reflect anything from a mild infection to chronic inflammatory conditions or cardiovascular risk. Levels above 10 mg/dL suggest a more significant inflammatory process, and readings above 50 mg/dL point to severe inflammation, often from acute infection or a major autoimmune flare.
CRP is a useful general indicator but not a diagnostic tool on its own. It tells you that inflammation exists somewhere in the body without pinpointing the source. That’s why it’s typically used alongside other tests and a clinical evaluation to identify the underlying cause.