Table 2.

Characteristics of included studies on animals.

Reference	Species	Study design	Sample	Therapy	Administration route	GI effects of treatment	Neurological effects of treatment
Chen et al. [30]	ASD mouse model	Saline group (C); maternal immune activation mice offspring(M); gut microbiota group: original donor (M + F); vitro cultured donor (C + F)	C: 5 M: 10 M + F: 7 C + F: 8	Gut microbiota transplantation	Gastric route	Significantly modified several key differential taxa in gut microbial composition	Assessed by behavioural assessment (open field, three-chamber social, marble burying, and self-grooming) and serum levels of chemokines GMT treatment with original and cultured donor gut microbiota significantly ameliorated anxiety-like and repetitive behaviours
Goo et al. [31]	Normal mice and Fmr1 KO mouse model	Animal model	NA	FMT	Gastric route	None	FMT ameliorated autistic-like behaviours, especially memory deficits and social withdrawal by several behavioural tests
Sharon et al. [32]	GF WT mice	Offspring of mice with FMT from human ASD patients Relevant groups: (all GF WT mice) FMT: (1) Offspring human mild ASD-FMT (2) Offspring human ASD-FMT (3) Offspring human ND-FMT	14–121 per group	FMT	Oral gavage	No differences in intestinal barrier function or cytokines from ileum or colon between group 2 and group 3	Assessed by marble burying (MB), open-field testing (OFT), and ultrasonic vocalization (USV), and the three-chamber sociability test (CST) MB, OFT, and USV: group 2 vs. other groups: more ASD-like behavioural deficits. 3-CST: no differences. DSI: decreased in group 2 vs. 3. Alternative splicing pattern of ASD-relevant genes in brains of group 2 vs. 3
Aabed et al. [33]	PPA hamster model	Animal model: FMT: (1) PPA + N-FMT No FMT: (2) Control (3) PPA (4) Clindamycin (5) PPA + bee pollen (6) PPA + Propolis	10 per group	FMT	Anorectally	NA	More oxidative stress in brains of group 3 and 4 vs. all other groups