A mushroom-fed faecal transplant undid antibiotic gut damage in mice

Almost everyone has taken a course of antibiotics and noticed their digestion was not the same for weeks afterward. The uncomfortable part is that there is very little evidence-based advice about what to do next. A new mouse study takes an unusual run at the problem: it feeds one group of mice a mushroom-derived carbohydrate, then transfers only the faeces from those mice into a second, untreated group. The second group recovered nearly as well as the first. Whatever the mushroom did, it did it through the bacteria, and the bacteria alone were enough to carry the benefit.

Key Takeaways

• Faecal microbiota transplant from mice given Agrocybe cylindracea polysaccharide reversed ciprofloxacin-induced gut dysbiosis in recipient mice, nearly matching the polysaccharide itself.
• The inflammatory cytokine IL-17 fell from 119.0 pg/mL in antibiotic-treated mice to 44.97 pg/mL after the transplant, while the beneficial Lachnospiraceae-NK4A136 group rose more than fourfold.
• Because the benefit transferred through faeces alone, the causal chain runs through the microbiome rather than through any direct effect of the mushroom compound on the animal.
• This is a mouse study with eight animals per group, and it is not a reason to buy mushroom supplements. The authors received no financial support for the work.

Agrocybe cylindracea polysaccharide FMT reversed antibiotic dysbiosis in mice

A faecal transplant taken from mice fed a mushroom polysaccharide restored gut bacterial diversity, reduced inflammation and repaired intestinal barrier markers in mice whose microbiomes had been damaged by ciprofloxacin, according to a study published on 13 July 2026 in Frontiers in Immunology. The work, by Aamna Atta, Muhammad Naveed, Bin Feng and colleagues, compared the polysaccharide given directly against a transplant of faeces from polysaccharide-fed donors, and found the two approaches produced broadly similar recoveries.

The polysaccharide (a long chain of linked sugar molecules, in this case extracted from the fruiting bodies of the Agrocybe cylindracea mushroom with hot water) was 87.13% glucose by monosaccharide composition, with smaller amounts of galactose, glucuronic acid and mannose. That matters because the mouse does not digest it; it reaches the colon intact, where bacteria ferment it. The transplant arm is the clean test of that assumption.

Post-antibiotic gut disruption is a problem millions of people actually have

Anyone who has taken a fluoroquinolone or a broad-spectrum antibiotic and then struggled with months of loose stools, bloating or new food sensitivities is the person this line of research is aimed at. The scale is not small: the US Centers for Disease Control and Prevention states that "at least 28% of antibiotics prescribed in outpatient settings are considered unnecessary," and that outpatient settings account for 85 to 95% of human antibiotic use. That is a very large number of disrupted microbiomes, many of them avoidable.

The finding is also relevant to people with inflammatory bowel disease, because the study's headline immune result centres on IL-17, a cytokine deeply implicated in intestinal inflammation. Its role is genuinely contested: a Mucosal Immunology commentary titled "IL-17: intestinal effector or protector?" laid out evidence that IL-17 may in some contexts limit rather than drive inflammation. So a drop in IL-17 should be read as a meaningful shift in immune tone, not automatically as a cure signal.

A natural-recovery control group is what makes this study credible

The design included a group that got antibiotics and then simply nothing, which is the comparison most studies of this kind skip. Male BALB/c mice aged four to five weeks were divided into five groups of eight: a normal control, a ciprofloxacin group, a natural-recovery group, a polysaccharide-treated group, and a transplant group. Ciprofloxacin was given orally at 50 mg/kg once daily for 14 days. From day 15 to day 28, mice received either the polysaccharide or a daily 200-microlitre oral gavage of faecal slurry, prepared at 160 mg of faeces per millilitre of chilled saline, from donors that had been given the polysaccharide alongside the antibiotic.

Letting the natural-recovery group run is what turns the result from "mice got better over two weeks" into something interpretable. They did not fully get better. Shannon diversity ranked normal control highest, then polysaccharide, then transplant, then natural recovery, with the ciprofloxacin group lowest, and at the phylum level the natural-recovery group remained badly skewed: Firmicutes at 9.77% and Proteobacteria at 36.86%, close to the untreated ciprofloxacin group's 11.64% and 42.25%. The transplant group, by contrast, reached 39.64% Firmicutes and pulled Proteobacteria down to 15.07%.

IL-17 and Lachnospiraceae moved together in the transplant group

The immune and bacterial changes tracked each other, which is the part that makes the mechanism plausible rather than coincidental. IL-17 in the ciprofloxacin group sat at 119.0 ± 16.25 pg/mL; natural recovery brought it to 82.34 pg/mL, while the polysaccharide brought it to 35.31 pg/mL and the transplant to 44.97 ± 4.39 pg/mL (p<0.001 and p<0.01 respectively versus ciprofloxacin). TNF-alpha fell from 170.7 to 84.18 pg/mL in the transplant group, IL-1 beta from 181.3 to 92.42 pg/mL, and IL-6 from 59.45 to 31.85 pg/mL. The anti-inflammatory cytokine IL-10 moved the other way, rising from 132.4 pg/mL to 202.0 pg/mL in transplant recipients (p<0.01).

On the bacterial side, the Lachnospiraceae-NK4A136 group, depleted to 4.08 ± 0.43 in ciprofloxacin-treated mice, recovered to 18.64 ± 1.03 after transplant and 33.71 ± 0.40 with the polysaccharide (p<0.001). Lachnospiraceae matter because members of the family produce butyrate, a short-chain fatty acid that feeds colon cells; supplementing butyrate-producing bacteria has been shown to improve epithelial barrier integrity in vitro using microbiota from Crohn's disease patients. Consistent with that, the transplant group showed restored mucin-2 production and tight junction protein expression compared with untreated antibiotic-exposed mice (p<0.001).

This is not an argument for buying mushroom supplements

To be direct: nothing here supports taking an Agrocybe supplement, and the study does not test that. The two things that worked were a purified, characterised polysaccharide extracted under laboratory conditions and a faecal transplant, neither of which is available over the counter or equivalent to a capsule of dried mushroom powder. Commercial mushroom products vary enormously in polysaccharide content.

Faecal microbiota transplantation in humans is an established treatment for recurrent Clostridioides difficile infection and is regulated as such; it is not an approved therapy for general post-antibiotic gut disruption, and self-administration carries real infection risk. The defensible takeaway is about mechanism: fermentable carbohydrates appear to shape the post-antibiotic recovery trajectory through the bacteria they feed. That is a reasonable prompt for a conversation with a clinician about dietary fibre, not a reason to buy anything.

Missing SCFA measurements and no polysaccharide-only control

The authors name their own two main gaps. The study lacked "fecal short-chain fatty acid quantification and a dedicated ACP-only control group." Both matter. Without measuring short-chain fatty acids, the butyrate mechanism remains inferred from which bacteria expanded rather than demonstrated directly. Without a group receiving the polysaccharide without antibiotics, it is impossible to know what it does to an undisturbed gut.

Add the usual constraints: eight mice per group, all male, all one inbred strain, all young, over a 28-day window that says nothing about durability. Cytokine values for the healthy control group were not reported numerically in the text, so the comparisons above are relative to the antibiotic-treated group rather than to a normal baseline. And 16S sequencing identifies bacteria to genus level, not the strain level needed to say which organism did the work.

Human trials and SCFA measurement are the obvious next steps

The near-term follow-ups are cheap: measure the short-chain fatty acids, add the missing control arm, and test durability past 28 days. Beyond that, the interesting question is whether a defined mixture of the bacteria that expanded would work as well as whole donor stool, since a defined consortium is far easier to regulate and manufacture. Human work on this has not been done at scale, so the realistic horizon is years. One notable feature of this paper is the absence of any commercial stake: the funding statement declares that "financial support was not received for this work and/or its publication," and the authors reported no competing interests.

Common Questions

Should I eat Agrocybe mushrooms after antibiotics? The study did not test eating mushrooms. It used a hot-water-extracted, chemically characterised polysaccharide and a faecal transplant in mice, neither of which corresponds to eating the whole food or taking a supplement.

Why does it matter that the effect transferred through faeces? Because it isolates the mechanism. If faeces alone from treated donors reproduces most of the benefit in untreated recipients, the polysaccharide is working by reshaping the bacterial community rather than by acting directly on the animal's tissues.

Did the mice recover on their own without treatment? Only partially. The natural-recovery group still showed heavily skewed bacterial composition after 14 days, with Firmicutes at 9.77% and Proteobacteria at 36.86%, alongside markedly higher inflammatory cytokines than the treated groups.

Is faecal transplant available for post-antibiotic gut problems? Not as a routine treatment. It is used clinically for recurrent Clostridioides difficile infection under medical supervision, and there is no approved indication for general dysbiosis after antibiotics.

References

Aamna Atta, Muhammad Naveed, Jinting Liu, et al. (2026). Agrocybe cylindracea polysaccharides and polysaccharides-conditioned fecal microbiota transplantation similarly restore ciprofloxacin-induced microbial dysbiosis and improve intestinal barrier function: a comparative study. Frontiers in Immunology. https://doi.org/10.3389/fimmu.2026.1841989