Can You Take Antibiotics While on Immunotherapy?
Understand how antibiotics may interact with immunotherapy and why discussing treatment plans with your healthcare team is essential for optimal care.
Understand how antibiotics may interact with immunotherapy and why discussing treatment plans with your healthcare team is essential for optimal care.
Antibiotics and immunotherapy are both critical tools in modern medicine, but their interaction is an area of growing research. While antibiotics fight bacterial infections, they can also influence immune function in ways that may impact the effectiveness of immunotherapy.
Understanding how these medications interact is essential for patients undergoing cancer treatment or therapies that enhance immune responses. This article explores key considerations when using antibiotics alongside immunotherapy and highlights the importance of medical guidance in managing potential risks.
Antibiotics target bacterial pathogens by disrupting essential cellular processes. Their mechanisms include inhibiting cell wall synthesis, interfering with protein production, disrupting nucleic acid replication, and altering metabolic pathways. Beta-lactams, such as penicillins and cephalosporins, prevent bacteria from forming a functional cell wall, leading to structural instability and lysis. Fluoroquinolones inhibit bacterial enzymes necessary for DNA replication, effectively halting bacterial proliferation.
Beyond pathogen eradication, antibiotics can influence immune function by altering microbial communities and modulating immune signaling. Some, like macrolides, reduce pro-inflammatory cytokine production and suppress neutrophil activation. Tetracyclines inhibit enzymes involved in inflammation, affecting immune cell recruitment. While these effects may benefit inflammatory conditions, they could also interfere with immune responses critical to immunotherapy.
Certain antibiotics, particularly those affecting mitochondrial function, can impair dendritic cell maturation and antigen presentation, leading to suboptimal T-cell activation. This is especially relevant in immunotherapy, where strong T-cell responses are necessary for success. Additionally, antibiotics that disrupt bacterial-derived immune stimulants may weaken innate immune recognition, potentially diminishing overall immune response.
Immunotherapy enhances or modifies the body’s natural defenses to combat diseases like cancer. Different types function through distinct biological pathways, each with unique interactions with antibiotics.
Checkpoint inhibitors block regulatory proteins on immune cells, allowing them to recognize and attack abnormal cells more effectively. The most common targets are PD-1, PD-L1, and CTLA-4. Drugs such as pembrolizumab and nivolumab (PD-1 inhibitors) and ipilimumab (CTLA-4 inhibitor) are widely used in treating cancers like melanoma, lung cancer, and renal cell carcinoma.
These therapies prevent immune suppression, sustaining T-cell activity against tumors. However, they can also cause immune-related side effects, including inflammation in organs like the lungs (pneumonitis) and intestines (colitis). Research suggests antibiotic use before or during checkpoint inhibitor therapy may reduce treatment efficacy, though the exact mechanisms remain under investigation.
CAR T-cell therapy is a personalized immunotherapy in which a patient’s T cells are genetically modified to target cancer cells. This approach has been particularly effective in treating hematologic malignancies like B-cell acute lymphoblastic leukemia and diffuse large B-cell lymphoma. FDA-approved CAR T-cell therapies, including tisagenlecleucel and axicabtagene ciloleucel, have shown durable responses in relapsed or refractory cases.
The process involves extracting T cells, engineering them to recognize tumor-associated antigens (such as CD19 in B-cell cancers), and reinfusing them to initiate a targeted immune attack. While highly effective, CAR T-cell therapy carries risks such as cytokine release syndrome (CRS) and neurotoxicity, requiring close monitoring. The impact of antibiotics on CAR T-cell therapy is under investigation, particularly regarding their influence on immune cell expansion and persistence.
Cytokine therapy involves administering signaling proteins that regulate immune activity. Interleukin-2 (IL-2) and interferon-alpha (IFN-α) are commonly used in cancer treatment. High-dose IL-2 is employed in metastatic melanoma and renal cell carcinoma, while IFN-α is used for certain leukemias and viral infections. These therapies stimulate immune cell proliferation and enhance cytotoxic activity against abnormal cells.
Despite their benefits, cytokine therapies can trigger systemic inflammatory responses, causing flu-like symptoms, hypotension, and vascular leak syndrome. Antibiotics may be necessary for treating infections that arise due to immune activation or therapy-related complications. However, their direct effect on cytokine therapy efficacy remains less understood compared to other immunotherapy types.
The human microbiome, particularly gut bacteria, plays a crucial role in maintaining physiological balance. Antibiotics, while essential for treating infections, significantly alter microbial communities by reducing beneficial bacteria. The extent of these changes depends on antibiotic class, dosage, duration, and individual microbiome diversity. Broad-spectrum antibiotics, such as fluoroquinolones and beta-lactams, cause the most pronounced disruptions, often leading to a sharp decline in microbial diversity.
This disruption can result in dysbiosis, where beneficial bacteria decline, allowing opportunistic pathogens to thrive. A reduction in genera like Bifidobacterium and Lactobacillus can create an environment favorable to harmful bacteria, such as Clostridioides difficile. Even short antibiotic courses can cause lasting shifts in microbial composition, with some species failing to recover for months or years. The loss of microbial diversity alters metabolic pathways, including the production of short-chain fatty acids like butyrate, which support gut integrity and immune regulation.
Antibiotics also influence microbiome function by altering enzymatic activity and gene expression. Some promote the expansion of antibiotic-resistant strains, which persist long after treatment. Changes in bacterial metabolism can affect nutrient absorption and bile acid processing, potentially leading to gastrointestinal issues like diarrhea or bloating. The degree of microbiome disruption varies among individuals based on diet, genetics, and prior antibiotic exposure.
Effective communication with healthcare providers is essential when managing antibiotics alongside immunotherapy. Oncologists, infectious disease specialists, and pharmacists evaluate potential drug interactions, determine appropriate antibiotic selection, and minimize unintended consequences. Since immunotherapy is highly individualized, healthcare teams assess factors like cancer type, disease progression, and treatment history before recommending antibiotics.
Timing matters, as studies suggest antibiotic use within 60 days of starting immunotherapy may affect treatment outcomes. Patients should disclose all medications, including over-the-counter drugs and supplements, to ensure coordinated care.
Clinicians weigh the risks and benefits when prescribing antibiotics. While bacterial infections must be treated promptly, unnecessary or prolonged antibiotic use can disrupt microbial balance. When possible, narrow-spectrum antibiotics are preferred to minimize microbiome disruption. Probiotic supplementation or dietary modifications may also be recommended to support gut health during antibiotic therapy. Regular monitoring through blood tests, stool analysis, or imaging helps track infection resolution and potential treatment-related side effects.