Nicotine, Inflammation and the Immune System

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1. Research at a Glance
2. The Papers
3. PubMed Topic Searches
4. More Nicotine Research
5. Connections
6. Featured Videos

Research at a Glance

What kind of study each paper on this page is, and when the papers were published. Hover over a bar for its count.

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The Papers (11)

Newest first. Study types on this page — Animal study: 9 · Cell study: 2. Each summary is written from the paper’s own abstract; follow the PubMed link for the full record.

Nicotine self-administration suppresses both pro- and anti-inflammatory accumbens cytokines but does not induce apoptosis in female rats

Animal study, 2026. This study used female rats that gave themselves nicotine, compared with rats that gave themselves saline, and measured immune signalling molecules (cytokines) in the ventral striatum, part of the brain's reward pathway, and in the blood. In the brain, inflammatory cytokines were suppressed, TNF-alpha most strongly. Fractalkine, a distress signal that nerve cells send out, went up, and the researchers found no sign of nerve cell death. In the blood, cytokine levels were mostly unchanged apart from a rise in TNF-alpha, so the authors conclude that chronic nicotine use in female rats may disrupt the normal immune balance in this brain region. These results come from rats only.

White AM, Richie DL, Kendrick PT et al. (2026). Nicotine self-administration suppresses both pro- and anti-inflammatory accumbens cytokines but does not induce apoptosis in female rats. Addict Neurosci. — PubMed PMID: 42808018 · doi:10.1016/j.addicn.2026.100263

Protective effects of nicotine with or without PPAR-γ inhibition in saline lavage-induced lung injury in rats

Animal study, 2026. This study in 50 male rats looked at whether nicotine protects the lungs in an experimental model of acute respiratory distress syndrome (ARDS), a severe lung injury, which the researchers caused by repeatedly washing the lungs with salt water. In these rats, nicotine improved blood pressure and circulation, oxygen exchange and lung mechanics. It also reduced the number of inflammatory white blood cells in the lungs, fluid build-up in the lungs and blood levels of nitric oxide by-products. When the researchers blocked a cell signalling pathway called PPAR-γ, several of these protective effects became weaker, although nicotine still helped partly, which suggests the two pathways may work together. These results come from rats only and have not been tested in people.

Fatemikia H, Ziaian B, Ketabchi F (2026). Protective effects of nicotine with or without PPAR-γ inhibition in saline lavage-induced lung injury in rats. Respir Physiol Neurobiol. — PubMed PMID: 42800496 · doi:10.1016/j.resp.2026.104651

Inhaled aerosolized nicotine suppresses the lung eosinophilic response to house dust mite allergen

Animal study, 2020. Researchers tested how breathing in nicotine affects the lung's allergic reaction to house dust mite in mice. Mice that inhaled aerosolized nicotine twice a day, 5 days a week for 8 weeks had far fewer eosinophils, a type of allergy-related white blood cell, in their lungs after allergen exposure, while nicotine given by mouth had no effect. Drugs that boost the alpha-7 nicotinic receptor also blocked the eosinophil response, and lung immune cells studied in culture showed that activating this receptor switched off a signal (eotaxin 2) that draws eosinophils in. These results come only from mice and mouse cells, and the authors suggest that the allergic response may be substantially changed in people who use e-cigarettes.

Gahring LC, Myers EJ, Rogers SW (2020). Inhaled aerosolized nicotine suppresses the lung eosinophilic response to house dust mite allergen. Am J Physiol Lung Cell Mol Physiol. — PubMed PMID: 32726138 · doi:10.1152/ajplung.00227.2020

Nicotine drives neutrophil extracellular traps formation and accelerates collagen-induced arthritis

Animal study, 2017. Researchers looked at neutrophil extracellular traps (NETs), which are web-like strands of DNA that a type of white blood cell called a neutrophil throws out. They studied this in blood cells from smokers and non-smokers, and in mice with a lab model of rheumatoid arthritis. Neutrophils from smokers formed more NETs. When nicotine was added in the lab to neutrophils from healthy non-smokers, they formed more NETs as the dose went up, and this worked through the alpha-7 nicotinic receptor on those cells. In the mice, nicotine made the arthritis worse and raised blood markers of NETs, so the authors suggest that nicotine-containing products, including e-cigarettes, may be harmful for people with rheumatoid arthritis.

Lee J, Luria A, Rhodes C et al. (2017). Nicotine drives neutrophil extracellular traps formation and accelerates collagen-induced arthritis. Rheumatology (Oxford). — PubMed PMID: 28013195 · doi:10.1093/rheumatology/kew449

Chronic nicotine treatment decreases LPS signaling through NF-κB and TLR-4 modulation in the hippocampus

Animal study, 2017. This study looked at whether giving nicotine daily for 14 days changes inflammation in the hippocampus, a memory area of the brain that has many nicotinic receptors, especially the alpha-7 type. The animals were then exposed to LPS, a piece of bacteria that triggers inflammation. In the animals given nicotine, LPS switched on less of NF-kB, an inflammation 'master switch', and less of the inflammation genes Tnf, Il1b, Nos2 and Tlr4. Drugs that block nicotinic receptors, including one that blocks only the alpha-7 type, cancelled this effect, which suggests nicotine acts through these receptors; the result comes from animals only, not from people.

Café-Mendes CC, Garay-Malpartida HM, Malta MB et al. (2017). Chronic nicotine treatment decreases LPS signaling through NF-κB and TLR-4 modulation in the hippocampus. Neurosci Lett. — PubMed PMID: 27984197 · doi:10.1016/j.neulet.2016.10.056

Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis

Animal study, 2016. In mice with an animal model of multiple sclerosis (experimental autoimmune encephalomyelitis), researchers tested whether nicotine could change the numbers of inflammatory immune cells (proinflammatory monocytes and neutrophils) entering the brain and spinal cord. Nicotine significantly reduced the infiltration of these cells into the central nervous system at the time points when they normally drive disease damage, acting through two nicotinic receptor subtypes (alpha7 and alpha9). Nicotine-treated mice also had lower levels of two chemical signals (CCL2 and CXCL2) in the brain that normally attract these inflammatory cells, and this drop occurred before the cell infiltration became severe.

Jiang W, St-Pierre S, Roy P et al. (2016). Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis. J Immunol. — PubMed PMID: 26810225 · doi:10.4049/jimmunol.1501613

Inflammation-induced increase in nicotinic acetylcholine receptor current in cutaneous nociceptive DRG neurons from the adult rat

Animal study, 2015. Researchers studied nerve cells from the skin-sensing ganglia of rats, looking at receptors that respond to nicotine. Nicotine-triggered electrical currents were found in about 70% of these nerve cells, with two distinct current types linked to different receptor subtypes. In rats with induced inflammation, both current types became stronger and more nerve cells showed the faster current type, suggesting these nicotine-responsive receptors may play a complex role in pain sensitivity during inflammation.

Zhang XL, Albers KM, Gold MS (2015). Inflammation-induced increase in nicotinic acetylcholine receptor current in cutaneous nociceptive DRG neurons from the adult rat. Neuroscience. — PubMed PMID: 25453771 · doi:10.1016/j.neuroscience.2014.10.018

Nicotine, an α7 nAChR agonist, reduces lipopolysaccharide-induced inflammatory responses and protects fetuses in pregnant rats

Animal study, 2014. This study tested nicotine, which acts on a nicotinic receptor (the alpha-7 receptor) linked to calming inflammation, in pregnant rats given a bacterial toxin that triggers a strong inflammatory response, with 6 rats per group. The toxin sharply raised the inflammatory signals TNF-alpha and IL-6 in the mothers' blood, and rats pretreated with nicotine injections for two days beforehand had significantly lower levels of both, while the anti-inflammatory signal IL-10 did not change. The toxin also reduced the number of live pups and their weights, and nicotine pretreatment significantly reversed both changes. These results are only in rats.

Yang J, Shi SQ, Shi L et al. (2014). Nicotine, an α7 nAChR agonist, reduces lipopolysaccharide-induced inflammatory responses and protects fetuses in pregnant rats. Am J Obstet Gynecol. — PubMed PMID: 24769008 · doi:10.1016/j.ajog.2014.04.026

Effect of nicotine on advanced glycation end product-induced immune response in human monocytes

Cell study, 2010. Researchers exposed human monocyte cells to advanced glycation end products (AGEs), substances formed when sugars attach to proteins or fats, which normally trigger inflammatory markers and immune activation. They found that nicotine blocked these AGE-triggered effects by acting on a specific nicotine receptor (alpha7-nAChR) on the cells. Blocking that receptor reversed nicotine's inhibitory effect, and nicotine was also shown to raise levels of certain signaling molecules (prostaglandin E2 and cAMP) that appear to be part of how it dampens the AGE response. This is a laboratory cell study, not a test in animals or people.

Takahashi HK, Liu K, Wake H et al. (2010). Effect of nicotine on advanced glycation end product-induced immune response in human monocytes. J Pharmacol Exp Ther. — PubMed PMID: 19955489 · doi:10.1124/jpet.109.160861

The immunosuppressive effects of nicotine during human mixed lymphocyte reaction

Cell study, 2007. This lab study used a test where human white blood cells from different people are mixed together, which mimics the immune reaction behind organ transplant rejection. The cells were stimulated with the inflammatory signal IL-18 and treated with nicotine at concentrations from 0.1 to 100 micromolar for 48 hours. Nicotine reduced the immune cells' contact molecules, cut production of the inflammatory messengers interferon-gamma and IL-12, and slowed the multiplication of immune cells. Half of these effects were reached at about 1 to 2 micromolar. Drugs that block the alpha7 nicotinic receptor cancelled these effects, and the authors suggest that prostaglandin E2, which nicotine increased, is partly involved. These results come from cells in a dish only.

Takahashi HK, Iwagaki H, Hamano R et al. (2007). The immunosuppressive effects of nicotine during human mixed lymphocyte reaction. Eur J Pharmacol. — PubMed PMID: 17254563 · doi:10.1016/j.ejphar.2006.12.003

Effect of nicotine on the immune system: possible regulation of immune responses by central and peripheral mechanisms

Animal study, 1998. This paper reviews earlier findings and reports new experiments on nicotine and immune function. In mice, chronic nicotine treatment reduced the inflammatory response in a turpentine-induced abscess model and was linked to lower death rates from acute influenza A lung infection in nicotine-treated mice. In rats, small doses of nicotine given directly into the brain (but not the same amount given elsewhere in the body) lowered antibody responses to a test antigen. In cell experiments, adding nicotine to T cells increased an enzyme called protein tyrosine kinase and raised calcium levels inside the cells. The authors conclude nicotine can affect immune responses both by acting directly on T cells and through effects on the brain that then influence the immune system.

Sopori ML, Kozak W, Savage SM et al. (1998). Effect of nicotine on the immune system: possible regulation of immune responses by central and peripheral mechanisms. Psychoneuroendocrinology. — PubMed PMID: 9621398 · doi:10.1016/s0306-4530(97)00076-0

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PubMed Topic Searches

1. PubMed: Inflammation and Immunity and nicotine (the search this page is built from)

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Connections

• Inflammation & How It Resolves — interactive animation
• Nicotine: The Research
• The Nicotine Patch, animated
• Nicotinic Acetylcholine Receptors
• Cigarette Smoke — what burnt tobacco adds that nicotine alone does not
• Brain and Memory
• Mood and Mental Health
• Cancer Research
• Heart and Blood Vessels
• Metabolism and Weight
• Addiction and Withdrawal
• Patches, Gum and Delivery
• Toxicity and Safety

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